Part 7: Adult Advanced Cardiovascular Life Support

Web-based Integrated 2015 & 2018 American Heart Association Guidelines for CPR and ECC

    Key Words:
  • arrhythmia
  • cardiac arrest
  • drugs
  • ventricular arrhythmia
  • ventricular fibrillation
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2018 Summary of Key Issues and Major Changes

The review considered the use of Amiodarone, Lidocaine, Magnesium and Beta-blockers for antiarrhythmic therapy during and immediately after adult ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) cardiac arrest. As a result, the Adult writing group’s recommendations for CPR and ECC have been updated and now provide further clarity regarding the application of antiarrhythmics during cardiac arrest. The recommendations are as follows:

Adult Recommendations

  • Use of antiarrhythmic drugs during resuscitation from adult VF/pVT cardiac arrest
    • 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.
    • The routine use of magnesium for cardiac arrest is not recommended in adult patients. Magnesium may be considered for torsades de pointes (ie, polymorphic VT associated with long-QT interval). The wording of this recommendation is consistent with the AHA’s 2010 Guidelines.
  • Use of antiarrhythmic drugs immediately following return of spontaneous circulation (ROSC) following adult cardiac arrest
    • There is insufficient evidence to support or refute the routine use of a β- blocker early (within the first hour) after ROSC.
    • There is insufficient evidence to support or refute the routine use of lidocaine early (within the first hour) after ROSC.

Antiarrhythmic Drugs Immediately After ROSC Following Adult Cardiac Arrest: β-Blocker Recommendation

2018 (Updated): There is insufficient evidence to support or refute the routine use of a β-blocker early (within the first hour) after ROSC.

2015 (Old): There is inadequate evidence to support the routine use of a β-blocker after cardiac arrest. However, the initiation or continuation of an oral or intravenous β-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT (Class IIb, LOE C-LD).

Why: The 2018 CoSTR summary and systematic review considered the use of prophylactic antiarrhythmic drugs immediately (within the first hour) after ROSC. Although no new studies were reviewed for this topic, detailed evaluation of the literature led to the simplification of the recommendation. There is no Class or LOE listed because the writing group agreed that there was insufficient evidence to make any recommendation.

Antiarrhythmic Drugs Immediately After ROSC Following Adult Cardiac Arrest: Lidocaine Recommendations

2018 (Updated): There is insufficient evidence to support or refute the routine use of lidocaine early (within the first hour) after ROSC. In the absence of contraindications, the prophylactic use of lidocaine may be considered in specific circumstances (such as during emergency medical services transport) when treatment of recurrent VF/pVT might prove to be challenging (Class IIb, LOE C-LD).

2015 (Old): There is inadequate evidence to support the routine use of lidocaine after cardiac arrest. However, the initiation or continuation of lidocaine may be considered immediately after ROSC from cardiac arrest due to VF/pVT (Class IIb, LOE C-LD).

Why: The 2018 CoSTR summary and systematic review considered the use of prophylactic antiarrhythmic drugs immediately (within the first hour) after ROSC. Although no new studies were reviewed for this topic, the writing group acknowledged that while there is insufficient evidence to support the routine use of lidocaine, there are situations for which recurrence of VF/pVT would be logistically challenging to manage (eg, during emergency medical services transport); in such situations, lidocaine administration may be considered.

Use of Antiarrhythmic Drugs During Resuscitation From Adult VF/pVT Cardiac Arrest: Amiodarone and Lidocaine Recommendation

2018 (Updated): 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).

2015 (Old): Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R). Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD).

Why: The 2018 CoSTR summary and systematic review considered the use of amiodarone or lidocaine during VF/pVT cardiac arrest refractory after at least 1 shock. The writing group evaluated a new large, out-of-hospital randomized controlled trial that compared a Captisol-based formulation of amiodarone with lidocaine or placebo for patients with refractory VF/pVT. Although the available studies did not demonstrate an improvement in survival to hospital discharge (or neurologically intact survival to discharge) associated with either drug, ROSC was higher in patients receiving lidocaine compared with placebo, and survival to hospital admission was higher with either drug compared with placebo. As a result, lidocaine is now recommended as an alternative to amiodarone and has now been added to the ACLS Cardiac Arrest Algorithm for treatment of shock-refractory VF/pVT (see the Figure 2 and ACLS Cardiac Arrest Algorithm Update section).

Use of Antiarrhythmic Drugs During Resuscitation From Adult VF/pVT Cardiac Arrest: Magnesium Recommendations

2018 (Updated): 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). The wording of this recommendation is consistent with the AHA’s 2010 ACLS guidelines.

2015 (Old): The routine use of magnesium for VF/pVT is not recommended in adult patients (Class III: No Benefit, LOE B-R).

2010 (Old): When VF/pVT cardiac arrest is associated with torsades de pointes, providers may administer IV/IO bolus of magnesium sulfate at a dose of 1 to 2 g diluted in 10 mL D5W (Class IIb, LOE C).

Why: The 2018 CoSTR summary and systematic review considered the use of magnesium during resuscitation from cardiac arrest. No new studies were reviewed for this topic, and only a handful of small, nonrandomized studies have been identified in past reviews. The current recommendation reaffirms that magnesium should not be routinely used for cardiac arrest and notes that it may be considered for the treatment of torsades de pointes (ie, polymorphic VT associated with long QT interval).

2015 Summary of Key Issues and Major Changes

Key issues and major changes in the 2015 Guidelines Update recommendations for advanced cardiac life support include the following:

  • The combined use of vasopressin and epinephrine offers no advantage to using standard-dose epinephrine in cardiac arrest. Also, vasopressin does not offer an advantage over the use of epinephrine alone. Therefore, to simplify the algorithm, vasopressin has been removed from the Adult Cardiac Arrest Algorithm–2015 Update.
  • Low end-tidal carbon dioxide (ETCO2) in intubated patients after 20 minutes of CPR is associated with a very low likelihood of resuscitation. While this parameter should not be used in isolation for decision making, providers may consider low ETCO2 after 20 minutes of CPR in combination with other factors to help determine when to terminate resuscitation.
  • Steroids may provide some benefit when bundled with vasopressin and epinephrine in treating IHCA. While routine use is not recommended pending follow-up studies, it would be reasonable for a provider to administer the bundle for IHCA.
  • When rapidly implemented, ECPR can prolong viability, as it may provide time to treat potentially reversible conditions or arrange for cardiac transplantation for patients who are not resuscitated by conventional CPR.
  • In cardiac arrest patients with nonshockable rhythm and who are otherwise receiving epinephrine, the early provision of epinephrine is suggested.
  • Studies about the use of lidocaine after ROSC are conflicting, and routine lidocaine use is not recommended. However, the initiation or continuation of lidocaine may be considered immediately after ROSC from VF/pulseless ventricular tachycardia (pVT) cardiac arrest.
  • One observational study suggests that ß-blocker use after cardiac arrest may be associated with better outcomes than when ß-blockers are not used. Although this observational study is not strong-enough evidence to recommend routine use, the initiation or continuation of an oral or intravenous (IV) ß-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT.

Vasopressors for Resuscitation: Vasopressin

2015 (Updated): Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest.

2010 (Old): One dose of vasopressin 40 units IV/ intraosseously may replace either the first or second dose of epinephrine in the treatment of cardiac arrest.

Why: Both epinephrine and vasopressin administration during cardiac arrest have been shown to improve ROSC. Review of the available evidence shows that efficacy of the 2 drugs is similar and that there is no demonstrable benefit from administering both epinephrine and vasopressin as compared with epinephrine alone. In the interest of simplicity, vasopressin has been removed from the Adult Cardiac Arrest Algorithm.

Vasopressors for Resuscitation: Epinephrine

2015 (New): It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm.

Why: A very large observational study of cardiac arrest with nonshockable rhythm compared epinephrine given at 1 to 3 minutes with epinephrine given at 3 later time intervals (4 to 6, 7 to 9, and greater than 9 minutes). The study found an association between early administration of epinephrine and increased ROSC, survival to hospital discharge, and neurologically intact survival.

ETCO2 for Prediction of Failed Resuscitation

2015 (New): In intubated patients, failure to achieve an ETCO2 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 should not be used in isolation.

Why: Failure to achieve an ETCO2 of 10 mm Hg by waveform capnography after 20 minutes of resuscitation has been associated with an extremely poor chance of ROSC and survival. However, the studies to date are limited in that they have potential confounders and have included relatively small numbers of patients, so it is inadvisable to rely solely on ETCO2 in determining when to terminate resuscitation.

Extracorporeal CPR

2015 (New): ECPR may be considered among select cardiac arrest patients who have not responded to initial conventional CPR, in settings where it can be rapidly implemented.

Why: Although no high-quality studies have compared ECPR to conventional CPR, a number of lower-quality studies suggest improved survival with good neurologic outcome for select patient populations. Because ECPR is resource intensive and costly, it should be considered only when the patient has a reasonably high likelihood of benefit—in cases where the patient has a potentially reversible illness or to support a patient while waiting for a cardiac transplant.


These Web-based Integrated Guidelines incorporate all relevant recommendations from 2010, 2015 and 2018. This 2018 American Heart Association (AHA) focused update on the advanced cardiovascular life support (ACLS) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) is based on the systematic review of antiarrhythmic therapy and the resulting “2018 International Consensus on CPR and ECC Science With Treatment Recommendations” (CoSTR) from the Advanced Life Support (ALS) Task Force of the International Liaison Committee on Resuscitation (ILCOR). The draft ALS CoSTR was posted online for public comment, and a summary containing the final wording of the CoSTR has been published simultaneously with this focused update. AHA guidelines and focused updates are developed in concert with the ILCOR systematic evidence review process. In 2015, the ILCOR process transitioned to a continuous one, with systematic reviews performed as new published evidence warrants them or when the ILCOR ALS Task Force prioritizes a topic. Once the ILCOR ALS Task Force develops a CoSTR statement, AHA ACLS science experts review the relevant topics and update the AHA’s ACLS guidelines as needed, typically on an annual basis. A description of the ILCOR continuous evidence review process is available in the 2017 CoSTR summary. The ILCOR systematic reviews use the Grading of Recommendations Assessment, Development, and Evaluation methodology and its associated nomenclature to determine the quality of evidence and strength of recommendations in the published CoSTR statement. The expert writing group for this 2018 ACLS guidelines focused update reviewed the studies and analysis of the 2018 CoSTR summary and carefully considered the ILCOR consensus recommendations in light of the structure and resources of the out-of-hospital and in-hospital resuscitation systems and the providers who use AHA guidelines. In addition, the writing group determined Classes of Recommendation and Levels of Evidence according to the most recent recommendations of the American College of Cardiology/AHA Task Force on Clinical Practice Guidelines (Table) by using the process detailed in “Part 2: Evidence Evaluation and Management of Conflicts of Interest” in the “2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” This 2018 ACLS guidelines focused update includes updates only to the recommendations for the use of antiarrhythmics during and immediately after adult ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) cardiac arrest. All other recommendations and algorithms published in “Part 7: Adult Advanced Cardiovascular Life Support” in the 2015 guidelines update and “Part 8: Adult Advanced Cardiovascular Life Support” in the “2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care” remain the official ACLS recommendations of the AHA ECC Science Subcommittee and writing groups. In addition, the “2017 American Heart Association Focused Update on Adult Basic Life Support and Cardiopulmonary Resuscitation Quality: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care” contains updated AHA recommendations for CPR delivered to adult patients in cardiac arrest. Through this systematic evaluation process, several issues have been identified in related areas that may be the subject of future systematic reviews.

Adjuncts to CPR - Updated

Oxygen Dose During CPR - Updated

The 2015 ILCOR systematic review considered inhaled oxygen delivery both during CPR and in the post–cardiac arrest period. This 2015 Guidelines Update evaluates the optimal inspired concentration of oxygen during CPR. The immediate goals of CPR are to restore the energy state of the heart so it can resume mechanical work and to maintain the energy state of the brain to minimize ischemic injury. Adequate oxygen delivery is necessary to achieve these goals. Oxygen delivery is dependent on both blood flow and arterial oxygen content. 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. Maximal inspired oxygen can be achieved with high-flow oxygen into a resuscitation bag device attached to a mask or an advanced airway.

2015 Evidence Summary

There were no adult human studies identified that directly compared maximal inspired oxygen with any other inspired oxygen concentration. However, 1 observational study of 145 OHCA patients evaluated arterial Po2 measured during CPR and cardiac arrest outcomes.1 In this study, during which all patients received maximal inspired oxygen concentration, patients were divided into low, intermediate, and high arterial Po2 ranges (less than 61, 61–300, and greater than 300 mmHg, respectively). The higher ranges of arterial Po2 during CPR were associated with an increase in hospital admission rates (low, 18.8%; intermediate, 50.6%; and high, 83.3%). However, there was no statistical difference in overall neurologic survival (low, 3.1%; intermediate, 13.3%; and high, 23.3%). Of note, this study did not evaluate the provision of various levels of inspired oxygen, so differences between groups likely reflect patient-level differences in CPR quality and underlying pathophysiology. This study did not find any association between hyperoxia during CPR and poor outcome.

2015 Recommendation - Updated

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

Evidence for detrimental effects of hyperoxia that may exist in the immediate post–cardiac arrest period should not be extrapolated to the low-flow state of CPR where oxygen delivery is unlikely to exceed demand or cause an increase in tissue Po2 . Therefore, until further data are available, physiology and expert consensus support providing the maximal inspired oxygen concentration during CPR.

Passive Oxygen Delivery During CPR

This topic was updated in 2015 and is discussed in Part 5: Adult Basic Life Support and Cardiopulmonary Resuscitation Quality.

Monitoring Physiologic Parameters During CPR - Updated

Monitoring both provider performance and patient physiologic parameters during CPR is essential to optimizing CPR quality. The 2010 Guidelines put a strong emphasis on CPR quality. In 2013, the AHA published a Consensus Statement focused on strategies to improve CPR quality.2 In 2015, the ILCOR ACLS Task Force evaluated the available clinical evidence to determine whether using physiologic feedback to guide CPR quality improved survival and neurologic outcome.

2015 Evidence Summary

Animal and human studies indicate that monitoring physiologic parameters during CPR provides valuable information about the patient’s condition and response to therapy. Most important, end-tidal CO2 (etco2 ), coronary perfusion pressure, arterial relaxation pressure, arterial blood pressure, and central venous oxygen saturation correlate with cardiac output and myocardial blood flow during CPR, and threshold values have been reported below which return of spontaneous circulation (ROSC) is rarely achieved.3-9 These parameters can be monitored continuously, without interrupting chest compressions. An abrupt increase in any of these parameters is a sensitive indicator of ROSC.10-27 There is evidence that these and other physiologic parameters can be modified by interventions aimed at improving CPR quality.3,28-39

The 2015 ILCOR systematic review was unable to identify any clinical trials that have studied whether titrating resuscitative efforts to a single or combined set of physiologic parameters during CPR results in improved survival or neurologic outcome.

2015 Recommendation - Updated

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)

Previous guidelines specified physiologic parameter goals; however, because the precise numerical targets for these parameters during resuscitation have not as yet been established, these were not specified in 2015.

Ultrasound During Cardiac Arrest - Updated

Bedside cardiac and noncardiac ultrasound are frequently used as diagnostic and prognostic tools for critically ill patients.40 Ultrasound may be applied to patients receiving CPR to help assess myocardial contractility and to help identify potentially treatable causes of cardiac arrest such as hypovolemia, pneumothorax, pulmonary thromboembolism, or pericardial tamponade.41 However, it is unclear whether important clinical outcomes are affected by the routine use of ultrasound among patients experiencing cardiac arrest.

2015 Evidence Summary

One limited study with a small sample size was identified that specifically addressed the utility of ultrasound during cardiac arrest. This study evaluated bedside cardiac ultrasound use during ACLS among adult patients in pulseless electrical activity arrest and found no difference in the incidence of ROSC when ultrasound was used.42

2015 Recommendations - Updated

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)

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)

Adjuncts for Airway Control and Ventilation - Updated

Overview of Airway Management

This section highlights recommendations for the support of ventilation and oxygenation during CPR and the peri-arrest period. The purpose of ventilation during CPR is to maintain adequate oxygenation and sufficient elimination of carbon dioxide. However, 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. Because both systemic and pulmonary perfusion are substantially reduced during CPR, normal ventilation-perfusion relationships can be maintained with a minute ventilation that is much lower than normal. During CPR with an advanced airway in place, a lower rate of rescue breathing is needed to avoid hyperventilation.

Ventilation and Oxygen Administration During CPR

During low blood flow states such as CPR, oxygen delivery to the heart and brain is limited by blood flow rather than by arterial oxygen content.43, 44 Therefore, rescue breaths are less important than chest compressions during the first few minutes of resuscitation from witnessed VF cardiac arrest and could reduce CPR efficacy due to interruption in chest compressions and the increase in intrathoracic pressure that accompanies positive-pressure ventilation.

Thus, during the first few minutes of witnessed cardiac arrest a lone rescuer should not interrupt chest compressions for ventilation. Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for VF cardiac arrest. (Class I, LOE C)

Bag-Mask Ventilation - Updated

Bag-mask ventilation is an acceptable method of providing ventilation and oxygenation during CPR but is a challenging skill that requires practice for continuing competency. All healthcare providers should be familiar with the use of the bag-mask device.45,46 Use of bag-mask ventilation is not recommended for a lone provider. When ventilations are performed by a lone provider, mouth-to-mouth or mouth-to-mask are more efficient. When a second provider is available, bag-mask ventilation may be used by a trained and experienced provider. But bag-mask ventilation is most effective when performed by 2 trained and experienced providers. One provider opens the airway and seals the mask to the face while the other squeezes the bag. Bag-mask ventilation is particularly helpful when placement of an advanced airway is delayed or unsuccessful. The desirable components of a bag-mask device are listed in “Part 5: Adult Basic Life Support and Cardiopulmonary Resuscitation Quality.

The provider should use an adult (1 to 2 L) bag and the provider should deliver approximately 600 mL of tidal volume sufficient to produce chest rise over 1 second.13 This volume of ventilation is adequate for oxygenation and minimizes the risk of gastric inflation. The provider should 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.

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.47-49

Bag-Mask Ventilation Compared With Any Advanced Airway During CPR - Updated

As stated above, bag-mask ventilation is a commonly used method for providing oxygenation and ventilation in patients with respiratory insufficiency or arrest. When cardiac arrest occurs, providers must determine the best way to support ventilation and oxygenation. Options include standard bag-mask ventilation versus the placement of an advanced airway (ie, endotracheal tube [ETT], supraglottic airway device [SGA]). Previous guidelines recommended that prolonged interruptions in chest compressions should be avoided during transitions from bag-mask ventilation to an advanced airway device. In 2015, ILCOR evaluated the evidence comparing the effect of bagmask ventilation versus advanced airway placement on overall survival and neurologic outcome from cardiac arrest.
2015 Evidence Summary

There is inadequate evidence to show a difference in survival or favorable neurologic outcome with the use of bag-mask ventilation compared with endotracheal intubation50-56 or other advanced airway devices.50,52-54,57 The majority of these retrospective observational studies demonstrated slightly worse survival with the use of an advanced airway when compared with bag-mask ventilation. However, interpretation of these results is limited by significant concerns of selection bias. Two additional observational studies57,58 showed no difference in survival.

Airway Adjuncts

Cricoid Pressure

Cricoid pressure in nonarrest patients may offer some measure of protection to the airway from aspiration and gastric insufflation during bag-mask ventilation.59-62 However, it also may impede ventilation and interfere with placement of a supraglottic airway or intubation.63-69 The role of cricoid pressure during out-of-hospital cardiac arrest and in-hospital cardiac arrest has not been studied. 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.

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

Oropharyngeal Airways

Although studies have not specifically considered the use of oropharyngeal airways in patients with cardiac arrest, airways may aid in the delivery of adequate ventilation with a bag-mask device by preventing the tongue from occluding the airway. Incorrect insertion of an oropharyngeal airway can displace the tongue into the hypopharynx, causing airway obstruction.

To facilitate delivery of ventilations 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)

Nasopharyngeal Airways

Nasopharyngeal airways are useful in patients with airway obstruction or those at risk for developing airway obstruction, particularly when conditions such as a clenched jaw prevent placement of an oral airway. Nasopharyngeal airways are better tolerated than oral airways in patients who are not deeply unconscious. Airway bleeding can occur in up to 30% of patients following insertion of a nasopharyngeal airway.70 Two case reports of inadvertent intracranial placement of a nasopharyngeal airway in patients with basilar skull fractures71,72 suggest that nasopharyngeal airways should be used with caution in patients with severe craniofacial injury.

As with all adjunctive equipment, safe use of the nasopharyngeal airway requires adequate training, practice, and retraining. No studies have specifically examined the use of nasopharyngeal airways in cardiac arrest patients. To facilitate delivery of ventilations with a bag-mask device, the nasopharyngeal airway can be used in patients with an obstructed airway.

In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred. (Class IIa, LOE C)

Advanced Airways - Updated

Ventilation with a bag and mask or with a bag through an advanced airway (eg, endotracheal tube or supraglottic airway) is acceptable during CPR. All healthcare providers should 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.

Providers must be aware of the risks and benefits of insertion of an advanced airway during a resuscitation attempt. Such risks are affected by the patient’s condition and the provider’s expertise in airway control. There are no studies directly addressing the timing of advanced airway placement and outcome during resuscitation from cardiac arrest. Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions, intubation frequently is associated with interruption of compressions for many seconds.

The provider should weigh the need for minimally interrupted compressions against the need for insertion of an endotracheal tube or supraglottic airway. There is inadequate evidence to define the optimal timing of advanced airway placement in relation to other interventions during resuscitation from cardiac arrest. In a registry study of 25 006 in-hospital cardiac arrests, earlier time to invasive airway (<5 minutes) was not associated with improved ROSC but was associated with improved 24-hour survival.73 In an urban out-of-hospital setting, intubation that was achieved in <12 minutes was associated with better survival than intubation achieved in ≥13 minutes.74

In out-of-hospital urban and rural settings, patients intubated during resuscitation had a better survival rate than patients who were not intubated,75 whereas in an in-hospital setting, patients who required intubation during CPR had a worse survival rate.76 A recent study77 found that delayed endotracheal intubation combined with passive oxygen delivery and minimally interrupted chest compressions was associated with improved neurologically intact survival after out-of-hospital cardiac arrest in patients with adult witnessed VF/pulseless VT.

If 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)

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.

To use advanced airways effectively, healthcare providers must maintain their knowledge and skills through frequent practice. It may be helpful for providers to master one primary method of airway control. Providers should have a second (backup) strategy for airway management and ventilation if they are unable to establish the first-choice airway adjunct. Bag-mask ventilation may serve as that backup strategy.

Once an advanced airway is inserted, providers should immediately perform a thorough assessment to ensure that it is properly positioned. This assessment should not interrupt chest compressions. Assessment by physical examination consists of visualizing chest expansion bilaterally and listening over the epigastrium (breath sounds should not be heard) and the lung fields bilaterally (breath sounds should be equal and adequate). A device also should be used to confirm correct placement (see the section “Endotracheal Intubation” below).

Providers should observe a persistent capnographic waveform with ventilation to confirm and monitor endotracheal tube placement in the field, in the transport vehicle, on arrival at the hospital, and after any patient transfer to reduce the risk of unrecognized tube misplacement or displacement.

The use of capnography to confirm and monitor correct placement of supraglottic airways has not been studied, and its utility will depend on airway design. However, effective ventilation through a supraglottic airway device should result in a capnograph waveform during CPR and after ROSC.

Once an advanced airway is in place, the 2 providers should no longer deliver cycles of CPR (ie, compressions interrupted by pauses for ventilation) unless ventilation is inadequate when compressions are not paused. Instead the compressing provider should give continuous chest compressions at a rate of 100/min to 120/min, without pauses for ventilation. The provider delivering ventilation should provide 1 breath every 6 seconds (10 breaths per minute). Providers should avoid delivering an excessive ventilation rate because doing so can compromise venous return and cardiac output during CPR. The 2 providers should change compressor and ventilator roles approximately every 2 minutes to prevent compressor fatigue and deterioration in quality and rate of chest compressions. When multiple providers are present, they should rotate the compressor role about every 2 minutes.

Advanced Airway Placement Choice - Updated

Advanced airway devices are frequently placed by experienced providers during CPR if bag-mask ventilation is inadequate or as a stepwise approach to airway management. Placement of an advanced airway may result in interruption of chest compressions, and the ideal timing of placement to maximize outcome has not been adequately studied. The use of an advanced airway device such as an ETT or SGA and the effect of ventilation technique on overall survival and neurologic outcome was evaluated in 2015.
2015 Evidence Summary
Endotracheal Intubation Versus Bag-Mask Ventilation - Updated

There is no high-quality evidence favoring the use of endotracheal intubation compared with bag-mask ventilation or an advanced airway device in relation to overall survival or favorable neurologic outcome.50-56 Evaluating retrospective studies that compare bag-mask ventilation to endotracheal intubation is challenging because patients with more severe physiologic compromise will typically receive more invasive care (including endotracheal intubation) than patients who are less compromised and more likely to survive. Within that context, a number of retrospective studies show an association of worse outcome in those who were intubated as compared with those receiving bag-mask ventilation. While the studies did attempt to control for confounders, bias still may have been present, limiting the interpretation of these investigations. These studies illustrate that endotracheal intubation can be associated with a number of complications and that the procedure requires skill and experience. Risks of endotracheal intubation during resuscitation include unrecognized esophageal intubation and increased hands-off time.
Supraglottic Airway Devices - Updated

Several retrospective studies compared a variety of supraglottic devices (laryngeal mask airway, laryngeal tube, Combitube, esophageal obturator airway) to both bag-mask ventilation and endotracheal intubation. There is no high-quality evidence demonstrating a difference in survival rate or favorable neurologic outcome from use of an SGA compared with bagmask ventilation50,52-54 or endotracheal intubation.50,52,53,57,78-83 Three observational studies demonstrated a lower rate of both overall survival and favorable neurologic outcome when SGA use was compared with bag-mask ventilation,50,52,54 whereas another observational study demonstrated similar survival rates.53

In studies comparing SGA insertion to endotracheal intubation, no high-quality studies have demonstrated a difference in overall survival or favorable neurologic outcome.53,57,78-80,83 Several retrospective observational studies show more favorable outcome with the use of an SGA device, whereas other studies favor the use of endotracheal intubation.50,52,53,81-83
2015 Recommendations - Updated

Either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting. (Class IIb, LOE C-LD)

For healthcare providers trained in their use, either an SGA device or an ETT may be used as the initial advanced airway during CPR. (Class IIb, LOE C-LD)

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.  Bag-mask ventilation also requires skill and proficiency.  The choice of bag-mask device versus advanced airway insertion, then, will be determined by the skill and experience of the provider.

Frequent experience or frequent retraining is recommended for providers who perform endotracheal intubation.73,84 (Class I, LOE B)

EMS systems that perform prehospital intubation should provide a program of ongoing quality improvement to minimize complications. (Class IIa, LOE B)

Clinical Assessment of Tracheal Tube Placement - Updated

The 2015 ILCOR systematic review considered tracheal tube placement during CPR. This section evaluates methods for confirming correct tracheal tube placement.

Attempts at endotracheal intubation during CPR have been associated with unrecognized tube misplacement or displacement as well as prolonged interruptions in chest compression. Inadequate training, lack of experience, patient physiology (eg, low pulmonary blood flow, gastric contents in the trachea, airway obstruction), and patient movement may contribute to tube misplacement. After correct tube placement, tube displacement or obstruction may develop. In addition to auscultation of the lungs and stomach, several methods (eg, waveform capnography, CO2 detection devices, esophageal detector device, tracheal ultrasound, fiberoptic bronchoscopy) have been proposed to confirm successful tracheal intubation in adults during cardiac arrest.
2015 Evidence Summary

The evidence regarding the use of tracheal detection devices during cardiac arrest is largely observational. Observational studies and 1 small randomized study of waveform capnography to verify ETT position in victims of cardiac arrest report a specificity of 100% for correct tube placement.85-87  Although the sensitivity of waveform capnography for detecting tracheal tube placement immediately after prehospital intubation was 100% in 1 study,85 several other studies showed that the sensitivity of waveform capnography decreases after a prolonged cardiac arrest. 85-87 Differences in sensitivity can be explained by the low pulmonary blood flow during cardiac arrest, which will decrease ETCO2 concentration.

Although exhaled CO2 detection suggests correct tracheal tube placement, false-positive results (CO2 detection with esophageal intubation) can occur after ingestion of carbonated liquids.66 False-negative results (ie, absent exhaled CO2 in the presence of tracheal intubation) can occur in the setting of pulmonary embolism, significant hypotension, contamination of the detector with gastric contents, and severe airflow obstruction.11,88,89 The use of CO2 -detecting devices to determine the correct placement of other advanced airways (eg, Combitube, laryngeal mask airway) has not been studied, but, as with an ETT, effective ventilation should produce a capnography waveform during CPR and after ROSC.

Colorimetric and nonwaveform CO2 detectors can identify the presence of exhaled CO2 from the respiratory tract, but there is no evidence that these devices are accurate for continued monitoring of ETT placement.11,85,90-94 Moreover, because a minimal threshold of CO2 must be reached to activate the detector and exhaled CO2 is low in cardiac arrest, proper placement of an ETT may not be confirmed with this qualitative methodology.

While observational studies and a small randomized controlled trial (RCT) of esophageal detector devices report a low false-positive rate for confirming tracheal placement, there is no evidence that these devices are accurate or practical for the continued monitoring of ETT placement.86-95,90,96,97

An ultrasound transducer can be placed transversely on the anterior neck above the suprasternal notch to identify endotracheal or esophageal intubation. In addition, ultrasound of the thoracic cavity can identify pleural movement as lung sliding. Unlike capnography, confirmation of ETT placement via ultrasonography is not dependent on adequate pulmonary blood flow and CO2 in exhaled gas.98-100 One small prospective study of experienced clinicians compared tracheal ultrasound to waveform capnography and auscultation during CPR and reported a positive predictive value for ultrasound of 98.8% and negative predictive value of 100%.100 The usefulness of tracheal and pleural ultrasonography, like fiberoptic bronchoscopy, may be limited by abnormal anatomy, availability of equipment, and operator experience.
2015 Recommendations - Updated

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

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

Postintubation Airway Management

After inserting and confirming correct placement of an endotracheal tube, the provider should record the depth of the tube as marked at the front teeth or gums and secure it. There is significant potential for endotracheal tube movement with head flexion and extension101-103 and when the patient is moved from one location to another.104,105 Continuous monitoring of endotracheal tube placement with waveform capnography is recommended as discussed above.

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

Devices and tape should be applied in a manner that avoids compression of the front and sides of the neck, which may impair venous return from the brain.

One out-of-hospital study106 and 2 studies in an intensive-care setting107,108 indicate that backboards, commercial devices for securing the endotracheal tube, and other strategies provide equivalent methods for preventing inadvertent tube displacement when compared with traditional methods of securing the tube (tape). These devices may be considered during patient transport. (Class IIb, LOE C)

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.

Ventilation After Advanced Airway Placement - Updated

The 2015 ILCOR systematic review addressed the optimal ventilation rate during continuous chest compressions among adults in cardiac arrest with an advanced airway. The 2015 Guidelines Update for ACLS applies only to patients who have been intubated and are in cardiac arrest. The effect of tidal volume and any other ventilation parameters during CPR are not addressed in this recommendation.

Except for respiratory rate, it is unknown whether monitoring ventilatory parameters (eg, minute ventilation, peak pressure) during CPR can influence outcome. However, positive pressure ventilation increases intrathoracic pressure and may reduce venous return and cardiac output, especially in patients with hypovolemia or obstructive airway disease. Ventilation at inappropriately high respiratory rates (greater than 25 breaths/ min) is common during resuscitation from cardiac arrest.109,110 There is concern that excessive ventilation in the setting of cardiac arrest may be associated with worse outcome.
2015 Evidence Summary

No human clinical trials were found addressing whether a ventilation rate of 10 breaths/min, compared with any other ventilation rate, changes survival with favorable neurologic or functional outcome. Although there have been a number of animal studies109,111-119 and 1 human observational study120 evaluating ventilation rates during CPR, the design and data from these studies did not allow for the assessment of the effect of a ventilation rate of 10 per minute compared with any other rate for ROSC or other outcomes.
2015 Recommendation - Updated

After placement of an advanced airway, it may be reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths/min) while continuous chest compressions are being performed. (Class IIb, LOE C-LD)

Automatic Transport Ventilators

In both out-of-hospital and in-hospital settings, automatic transport ventilators (ATVs) can be useful for ventilation of adult patients in noncardiac arrest who have an advanced airway in place. (Class IIb, LOE C)

There are very few studies evaluating the use of ATVs attached to advanced airways during ongoing resuscitative efforts.

During prolonged resuscitative efforts the use of an ATV (pneumatically powered and time- or pressure-cycled) may allow the EMS team to perform other tasks while providing adequate ventilation and oxygenation.121,122 (Class IIb, LOE C)

Providers should always have a bag-mask device available for backup.

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.

Management of Cardiac Arrest - Updated


This section details the general care of a patient in cardiac arrest and provides an overview of the ACLS Adult Cardiac Arrest Algorithms (Figure 1 and Figure 2). Cardiac arrest can be caused by 4 rhythms: ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), pulseless electric activity (PEA), and asystole. VF represents disorganized electric activity, whereas pulseless VT represents organized electric activity of the ventricular myocardium. Neither of these rhythms generates significant forward blood flow. PEA encompasses a heterogeneous group of organized electric rhythms that are associated with either absence of mechanical ventricular activity or mechanical ventricular activity that is insufficient to generate a clinically detectable pulse. Asystole (perhaps better described as ventricular asystole) represents absence of detectable ventricular electric activity with or without atrial electric activity.

Figure 1: Adult Cardiac Arrest Algorithm―2018 Update

Figure 2: ACLS Cardiac Arrest Circular Algorithm - 2018 Update

Survival from these cardiac arrest rhythms requires both basic life support (BLS) and a system of advanced cardiovascular life support (ACLS) with integrated post–cardiac arrest care. The foundation of successful ACLS is high-quality CPR, and, for VF/pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge.123-128 In comparison, other ACLS therapies such as some medications and advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge.73,75,129-133The majority of clinical trials testing these ACLS interventions, however, preceded the recently renewed emphasis on high-quality CPR and advances in post–cardiac arrest care (see “Part 8: Post–Cardiac Arrest Care”). Therefore, it remains to be determined if improved rates of ROSC achieved with ACLS interventions might better translate into improved long-term outcomes when combined with higher-quality CPR and post–cardiac arrest interventions such as therapeutic hypothermia and early percutaneous coronary intervention (PCI).

The ACLS Adult Cardiac Arrest Algorithms (Figure 1) are presented in the traditional box-and-line format and a new circular format. The 2 formats are provided to facilitate learning and memorization of the treatment recommendations discussed below. Overall these algorithms have been simplified and redesigned to emphasize the importance of high-quality CPR that is fundamental to the management of all cardiac arrest rhythms. Periodic pauses in CPR should be as brief as possible and only as necessary to assess rhythm, shock VF/VT, perform a pulse check when an organized rhythm is detected, or place an advanced airway. Monitoring and optimizing quality of CPR on the basis of either mechanical parameters (chest compression rate and depth, adequacy of relaxation, and minimization of pauses) or, when feasible, physiologic parameters (partial pressure of end-tidal CO2 [PETCO2], arterial pressure during the relaxation phase of chest compressions, or central venous oxygen saturation [ScvO2]) are encouraged (see “Monitoring During CPR” below). In the absence of an advanced airway, a synchronized compression–ventilation ratio of 30:2 is recommended at a compression rate of at least 100-120 per minute. After placement of a supraglottic airway or an endotracheal tube, the provider performing chest compressions should deliver at least 100-120 compressions per minute continuously without pauses for ventilation. The provider delivering ventilations should give 1 breath every 6 seconds (10 breaths per minute) and should be particularly careful to avoid delivering an excessive number of ventilations.

In addition to high-quality CPR, the only rhythm-specific therapy proven to increase survival to hospital discharge is defibrillation of VF/pulseless VT. Therefore, this intervention is included as an integral part of the CPR cycle when the rhythm check reveals VF/pulseless VT. Other ACLS interventions during cardiac arrest may be associated with an increased rate of ROSC but have not yet been proven to increase survival to hospital discharge. Therefore, they are recommended as considerations and should be performed without compromising quality of CPR or timely defibrillation. In other words, vascular access, drug delivery, and advanced airway placement should not cause significant interruptions in chest compression or delay defibrillation. There is insufficient evidence to recommend a specific timing or sequence (order) of drug administration and advanced airway placement during cardiac arrest. In most cases the timing and sequence of these secondary interventions will depend on the number of providers participating in the resuscitation and their skill levels. Timing and sequence will also be affected by whether vascular access has been established or an advanced airway placed before cardiac arrest.

Understanding the importance of diagnosing and treating the underlying cause is fundamental to management of all cardiac arrest rhythms. During management of cardiac arrest the provider should consider the H’s and T’s to identify and treat any factor that may have caused the arrest or may be complicating the resuscitative effort (Table 1).

Table 1: 2010 - Treatable Causes of Cardiac Arrest: The H's and T's

It is common for the arrest rhythm to evolve during the course of resuscitation. In such cases management should shift smoothly to the appropriate rhythm-based strategy. In particular, providers should be prepared to deliver a timely shock when a patient who presented with asystole or PEA is found to be in VF/pulseless VT during a rhythm check. There is no evidence that the resuscitation strategy for a new cardiac arrest rhythm should necessarily be altered based on the characteristics of the previous rhythm. Medications administered during resuscitation should be monitored and total doses tabulated to avoid potential toxicity.

If the patient achieves ROSC, it is important to begin post–cardiac arrest care immediately to avoid rearrest and optimize the patient’s chance of long-term survival with good neurologic function (see “Part 8: Post–Cardiac Arrest Care”). Finally, the reality is that the majority of resuscitative efforts do not result in ROSC. Criteria for ending unsuccessful resuscitative efforts are addressed in Part 3: Ethical Issues.

Rhythm-Based Management of Cardiac Arrest

In most cases of witnessed and unwitnessed cardiac arrest the first provider should start CPR with chest compressions and the second provider should get or turn on the defibrillator, place the adhesive pads or paddles, and check the rhythm. Paddles and electrode pads should be placed on the exposed chest in an anterior-lateral position. Acceptable alternative positions are anterior-posterior, anterior-left infrascapular, and anterior-right infrascapular. 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 be resumed immediately. If a cardiac monitor is attached to the patient at the time of arrest, the rhythm can be diagnosed before CPR is initiated.

VF/Pulseless VT

When a rhythm check by an automated external defibrillator (AED) reveals VF/VT, the AED will typically prompt to charge, “clear” the victim for shock delivery, and then deliver a shock, all of which should be performed as quickly as possible. CPR should be resumed immediately after shock delivery (without a rhythm or pulse check and beginning with chest compressions) and continue for 2 minutes before the next rhythm check.

When a rhythm check by a manual defibrillator reveals VF/VT, the first provider should resume CPR while the second provider charges the defibrillator. 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 immediately after shock delivery (without a rhythm or pulse check and beginning with chest compressions) and continues 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. CPR quality should be monitored based on mechanical or physiologic parameters (see “Monitoring During CPR” below).
Defibrillation Strategies for Ventricular Fibrillation or Pulseless Ventricular Tachycardia: Waveform Energy and First-Shock Success

Currently manufactured manual and automated external defibrillators use biphasic waveforms of 3 different designs: biphasic truncated exponential (BTE), rectilinear biphasic (RLB), and pulsed biphasic waveforms; they deliver different peak currents at the same programmed energy setting and may adjust their energy output in relation to patient impedance in differing ways. These factors can make comparisons of shock efficacy between devices from different manufacturers challenging even when the same programmed energy setting is used. A substantial body of evidence now exists for the efficacy of BTE and RLB waveforms, with a smaller body of evidence for the pulsed waveform. An impedance-compensated version of the pulsed biphasic waveform is now clinically available, but no clinical studies were identified to define its performance characteristics.
2015 Evidence Summary

There is no evidence indicating superiority of one biphasic waveform or energy level for the termination of ventricular fibrillation (VF) with the first shock (termination is defined as absence of VF at 5 seconds after shock). All published studies support the effectiveness (consistently in the range of 85%–98%)134 of biphasic shocks using 200 J or less for the first shock.134 Defibrillators using the RLB waveform typically deliver more shock energy than selected, based on patient impedance. Thus, in the single study in which a manufacturer’s nonescalating energy device was programmed to deliver 150 J shocks, comparison with other devices was not possible because shock energy delivery in other devices is adjusted for measured patient impedance. For the RLB, a selected energy dose of 120 J typically provides nearly 150 J for most patients.
2015 Recommendations - Updated

Defibrillators (using BTE, RLB, or monophasic waveforms) are recommended to treat atrial and ventricular arrhythmias. (Class I, LOE B-NR)

Based on their greater success in arrhythmia termination, defibrillators using biphasic waveforms (BTE or RLB) are preferred to monophasic defibrillators for treatment of both atrial and ventricular arrhythmias. (Class IIa, LOE B-R)

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)
Defibrillation Strategies for Ventricular Fibrillation or Pulseless Ventricular Tachycardia: Energy Dose for Subsequent Shocks

The 2010 Guidelines regarding treatment of VF/pulseless ventricular tachycardia (pVT) recommended that if the first shock dose did not terminate VF/pVT, the second and subsequent doses should be equivalent, and higher doses may be considered. The evidence supporting energy dose for subsequent shocks was evaluated for the 2015 Guidelines Update.
2015 Evidence Summary

Observational data indicate that an automated external defibrillator administering a high peak current at 150 J biphasic fixed energy can terminate initial, as well as persistent or recurrent VF, with a high rate of conversion.135 In fact, the high conversion rate achieved with all biphasic waveforms for the first shock makes it difficult to study the energy requirements for second and subsequent shocks when the first shock is not successful. A 2007 study attempted to determine if a fixed lower energy dose or escalating higher doses were associated with better outcome in patients requiring more than 1 shock. Although termination of VF at 5 seconds after shock was higher in the escalating higher-energy group (82.5% versus 71.2%), there were no significant differences in ROSC, survival to discharge, or survival with favorable neurologic outcome between the 2 groups. In this study, only 1 manufacturer’s nonescalating energy device, programmed to deliver 150-J shocks, was used. Thus, it is not possible to compare this 150-J shock with that delivered by any other device set to deliver 150 J.

There is a decline in shock success with repeated shocks. One nonrandomized trial that used a BTE waveform reported a decline in shock success when repeated shocks at the same energy were administered.136 For the RLB waveform, 1 observational study reported an initial VF termination rate of 87.8% at a selected energy setting of 120 J and an 86.4% termination rate for persistent VF. Recurrence of VF did not affect ultimate shock success, ROSC, or discharge survival.137
2015 Recommendations - Updated

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)

If using a manual defibrillator capable of escalating energies, higher energy for second and subsequent shocks may be considered. (Class IIb, LOE C-LD)
Defibrillation Strategies for Ventricular Fibrillation or Pulseless Ventricular Tachycardia: Single Shocks Versus Stacked Shocks

The 2010 Guidelines recommended a 2-minute period of CPR after each shock instead of immediate successive shocks for persistent VF. The rationale for this is at least 3-fold: First, VF is terminated with a very high rate of success with biphasic waveforms. Second, when VF is terminated, a brief period of asystole or pulseless electrical activity (PEA) typically ensues and a perfusing rhythm is unlikely to be present immediately. Third, this provides for a period of uninterrupted CPR following a shock before repeat rhythm analysis.  The evidence for single versus stacked shocks was reviewed again in 2015.
2015 Evidence Summary

One RCT that comprised 845 OHCA patients found no difference in 1-year survival when a single shock protocol with 2 minutes of CPR between successive shocks was compared against a previous resuscitation protocol employing 3 initial stacked shocks with 1 minute of CPR between subsequent shocks (odds ratio, 1.64; 95% confidence interval, 0.53– 5.06).138 An RCT published in 2010 showed no difference in frequency of VF recurrence when comparing the 2 treatment protocols.139 In that study, increased time in recurrent VF was associated with decreased favorable neurologic survival under either protocol.

There is evidence that resumption of chest compressions immediately after a shock can induce recurrent VF, but the benefit of CPR in providing myocardial blood flow is thought to outweigh the benefit of immediate defibrillation for the VF.140 Another study of patients presenting in VF after a witnessed arrest concluded that recurrence of VF within 30 seconds of a shock was not affected by the timing of resumption of chest compressions.141 Thus, the effect of chest compressions on recurrent VF is not clear. It is likely that in the future, algorithms that recognize recurrent VF during chest compressions with high sensitivity and specificity will allow us to deliver a shock earlier in the CPR cycle, thereby reducing the length of time the myocardium is fibrillating and the duration of postshock CPR.142
2015 Recommendation - Updated

A single-shock strategy (as opposed to stacked shocks) is reasonable for defibrillation. (Class IIa, LOE B-NR)
Automatic Versus Manual Modes for Multimodal Defibrillators

Use of a multimodal defibrillator in manual mode may reduce the duration of interruption of CPR required for rhythm analysis compared with automatic mode but could increase the frequency of inappropriate shock.143,144

Current evidence indicates that the benefit of using a multimodal defibrillator in manual instead of automatic mode during cardiac arrest is uncertain. (Class IIb, LOE C)
CPR Before Defibrillation
VF Waveform Analysis to Predict Defibrillation Success

Retrospective analysis of VF waveforms in multiple clinical studies suggests that it is possible to predict the success of defibrillation from the fibrillation waveform with varying reliability.145,146-165 No prospective human studies have specifically evaluated whether treatment altered by predicting success of defibrillation can improve successful defibrillation, rate of ROSC, or survival from cardiac arrest.

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)


When a rhythm check by an AED reveals a nonshockable rhythm, CPR should be resumed immediately, beginning with chest compressions, and should continue for 2 minutes before the rhythm check is repeated. When a rhythm check using a manual defibrillator or cardiac monitor reveals an organized rhythm, a pulse check is performed. If a pulse is detected, post–cardiac arrest care should be initiated immediately (see Part 8: Post–Cardiac Arrest Care). If the rhythm is asystole or the pulse is absent (eg, PEA), CPR should be resumed immediately, beginning with chest compressions, and should continue for 2 minutes before the rhythm check is repeated. The provider performing chest compressions should switch every 2 minutes. CPR quality should be monitored on the basis of mechanical or physiologic parameters (see “Monitoring During CPR” below).
Treating Potentially Reversible Causes of PEA/Asystole

PEA is often caused by reversible conditions and can be treated successfully if those conditions are identified and corrected. During each 2-minute period of CPR the provider should recall the H’s and T’s to identify factors that may have caused the arrest or may be complicating the resuscitative effort (see Table 1 and “Part 10: Special Circumstances of Resuscitation”). Given the potential association of PEA with hypoxemia, placement of an advanced airway is 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 will potentially benefit from administration of empirical IV/IO crystalloid. A patient with PEA caused by severe blood loss will potentially 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)

Finally, if tension pneumothorax is clinically suspected as the cause of PEA, initial management includes needle decompression. If available, echocardiography can be used to guide management of PEA because it provides useful information about intravascular volume status (assessing ventricular volume), cardiac tamponade, mass lesions (tumor, clot), left ventricular contractility, and regional wall motion.166 See “Part 10: Special Circumstances of Resuscitation” for management of toxicological causes of cardiac arrest.

Asystole is commonly the end-stage rhythm that follows prolonged VF or PEA, and for this reason the prognosis is generally much worse.
ROSC After PEA/Asystole

If the patient has ROSC, post–cardiac arrest care should be initiated (see Part 8: Post–Cardiac Arrest Care). Of particular importance is treatment of hypoxemia and hypotension and early diagnosis and treatment of the underlying cause of cardiac arrest.

Therapeutic hypothermia may be considered when the patient is comatose. (Class IIb, LOE C)

Medications for Arrest Rhythms

The primary goal of pharmacologic therapy during cardiac arrest is to facilitate restoration and maintenance of a perfusing spontaneous rhythm. Toward this goal, ACLS drug therapy during CPR is often associated with increased rates of ROSC and hospital admission but not increased rates of long-term survival with good neurologic outcome. One study 133 randomized patients to IV or no IV medications during management of adult out-of-hospital cardiac arrest. The study demonstrated higher rates of ROSC in the IV group (40% IV versus 25% no IV [odds ratio (OR) 1.99; 95% confidence interval (CI) 1.48 to 2.67]), but there was no statistical difference in survival to hospital discharge (10.5% IV versus 9.2% no IV [OR 1.16; 95% CI 0.74 to 1.82]) or survival with favorable neurologic outcome (9.8% IV versus 8.1% no IV [OR 1.24; 95% CI 0.77 to 1.98]). This study was not adequately powered to detect clinically important differences in long-term outcomes. Evidence from one nonrandomized trial 132 found that the addition of ACLS interventions including IV drugs in a previously optimized BLS system with rapid defibrillation resulted in an increased rate of ROSC (18.0% with ACLS versus 12.9% before ACLS, P<0.001) and hospital admission (14.6% with ACLS versus 10.9% before ACLS, P<0.001) but no statistical difference in survival to hospital discharge (5.1% with ACLS versus 5.0% before ACLS). Whether optimized high-quality CPR and advances in post–cardiac arrest care will enable the increased rates of ROSC with ACLS medications to be translated into increased long-term survival remains to be determined.

Ventricular Fibrillation (VF) or Pulseless Ventricular Tachycardia (pVT)
Treating Potentially Reversible Causes of VF/pVT

The importance of diagnosing and treating the underlying cause of VF/pVT is fundamental to the management of all cardiac arrest rhythms. As always, the provider should recall the H’s and T’s to identify a factor that may have caused the arrest or may be complicating the resuscitative effort (see Table 1 and “Part 10: Special Circumstances of Resuscitation”). In the case of refractory VF/pulseless VT, acute coronary ischemia or myocardial infarction should be considered as a potential etiology. Reperfusion strategies such as coronary angiography and PCI during CPR or emergency cardiopulmonary bypass have been demonstrated to be feasible in a number of case studies and case series but have not been evaluated for their effectiveness in RCTs.167-176 Fibrinolytic therapy administered during CPR for acute coronary occlusion has not been shown to improve outcome.177

If the patient has ROSC, post–cardiac arrest care should be started. Of particular importance are treatment of hypoxemia and hypotension, early diagnosis and treatment of ST-elevation myocardial infarction (STEMI) (Class I, LOE B)

and therapeutic hypothermia in comatose patients. (Class I, LOE B)

Antiarrhythmic Drugs During and Immediately After Cardiac Arrest - Updated

The 2015 ILCOR systematic review addressed whether the administration of antiarrhythmic drugs for cardiac arrest due to refractory VF or pVT results in better outcome.
Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: Antiarrhythmic Therapy for Refractory VF/pVT Arrest - Updated

Refractory VF/pVT refers to VF or pVT that persists or recurs after 1 or more shocks. It is unlikely that an antiarrhythmic drug will itself pharmacologically convert VF/pVT to an organized perfusing rhythm. Rather, 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. Some antiarrhythmic drugs have been associated with increased rates of ROSC and hospital admission, but none have yet been proven to increase long-term survival or survival with good neurologic outcome. Thus, establishing vascular access to enable drug administration should not compromise the quality of CPR or timely defibrillation, which are known to improve survival. The optimal sequence of ACLS interventions, including administration of antiarrhythmic drugs during resuscitation and the preferred manner and timing of drug administration in relation to shock delivery, is not known. Previous ACLS guidelines addressed the use of magnesium in cardiac arrest with polymorphic ventricular tachycardia (ie, torsades de pointes) or suspected hypomagnesemia, and this has not been reevaluated in the 2015 Guidelines Update. These previous guidelines recommended defibrillation for termination of polymorphic VT (ie, torsades de pointes), followed by consideration of intravenous magnesium sulfate when secondary to a long QT interval.

The 2015 ILCOR systematic review did not specifically address the selection or use of second-line antiarrhythmic medications in patients who are unresponsive to a maximum therapeutic dose of the first administered drug, and there are limited data available to direct such treatment.
2015 Evidence Summary
Amiodarone - Updated

Intravenous amiodarone is available in 2 approved formulations in the United States, one containing polysorbate 80, a vasoactive solvent that can provoke hypotension, and one containing captisol, which has no vasoactive effects. In blinded RCTs in adults with refractory VF/pVT in the out-of-hospital setting, paramedic administration of amiodarone in polysorbate (300 mg or 5 mg/kg) after at least 3 failed shocks and administration of epinephrine improved hospital admission rates when compared to placebo with polysorbate178 or 1.5 mg/kg lidocaine with polysorbate.179 Survival to hospital discharge and survival with favorable neurologic outcome, however, was not improved by amiodarone compared with placebo or amiodarone compared with lidocaine, although these studies were not powered for survival or favorable neurologic outcome.
Lidocaine - Updated

Intravenous lidocaine is an alternative antiarrhythmic drug of long-standing and widespread familiarity. Compared with no antiarrhythmic drug treatment, lidocaine did not consistently increase ROSC and was not associated with improvement in survival to hospital discharge in observational studies.180,181 In a prospective, blinded, randomized clinical trial, lidocaine was less effective than amiodarone in improving hospital admission rates after OHCA due to shock-refractory VF/pVT, but there were no differences between the 2 drugs in survival to hospital discharge.179
Procainamide - Updated

Procainamide is available only as a parenteral formulation in the United States. In conscious patients, procainamide can be given only as a controlled infusion (20 mg/min) because of its hypotensive effects and risk of QT prolongation, making it difficult to use during cardiac arrest. Procainamide was recently studied as a second-tier antiarrhythmic agent in patients with OHCA due to VF/pVT that was refractory to lidocaine and epinephrine. In this study, the drug was given as a rapid infusion of 500 mg (repeated as needed up to 17 mg/kg) during ongoing CPR. An unadjusted analysis showed lower rates of hospital admission and survival among the 176 procainamide recipients as compared with 489 nonrecipients. After adjustment for patients’ clinical and resuscitation characteristics, no association was found between use of the drug and hospital admission or survival to hospital discharge, although a modest survival benefit from the drug could not be excluded.182
Magnesium - Updated

Magnesium acts as a vasodilator and is an important cofactor in regulating sodium, potassium, and calcium flow across cell membranes. In 3 randomized clinical trials, magnesium was not found to increase rates of ROSC for cardiac arrest due to any presenting rhythm,183 including VF/pVT.184,185 In these RCTs and in 1 additional randomized clinical trial, the use of magnesium in cardiac arrest for any rhythm presentation of cardiac arrest183,186 or strictly for VF arrest184,185 did not improve survival to hospital discharge or neurologic outcome.186
Recommendations - Updated

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

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)

No antiarrhythmic drug has yet been shown to increase survival or neurologic outcome after cardiac arrest due to VF/pVT. Accordingly, recommendations for the use of antiarrhythmic medications in cardiac arrest are based primarily on the potential for benefit on short-term outcome until more definitive studies are performed to address their effect on survival and neurologic outcome.
Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: Antiarrhythmic Drugs After Resuscitation - Updated

The 2015 ILCOR systematic review addressed whether, after successful termination of VF or pVT cardiac arrest, the prophylactic administration of antiarrhythmic drugs for cardiac arrest results in better outcome. The only medications studied in this context are β-adrenergic blocking drugs and lidocaine, and the evidence for their use is limited.
2015 Evidence Summary
β-Adrenergic Blocking Drugs - Updated

β-Adrenergic blocking drugs blunt heightened catecholamine activity that can precipitate cardiac arrhythmias. The drugs also reduce ischemic injury and may have membrane-stabilizing effects. In 1 observational study of oral or intravenous metoprolol or bisoprolol during hospitalization after cardiac arrest due to VF/pVT, recipients had a significantly higher adjusted survival rate than nonrecipients at 72 hours after ROSC and at 6 months.187 Conversely, β-blockers can cause or worsen hemodynamic instability, exacerbate heart failure, and cause bradyarrhythmias, making their routine adminis- tration after cardiac arrest potentially hazardous. There is no evidence addressing the use of β-blockers after cardiac arrest precipitated by rhythms other than VF/pVT.
Lidocaine - Updated

Early studies in patients with acute myocardial infarction found that lidocaine suppressed premature ventricular complexes and nonsustained VT, rhythms that were believed to presage VF/pVT. Later studies noted a disconcerting association between lidocaine and higher mortality after acute myocardial infarction, possibly due to a higher incidence of asystole and bradyarrhythmias; the routine practice of administering prophylactic lidocaine during acute myocardial infarction was abandoned.188,189 The use of lidocaine was explored in a multivariate and propensity score–adjusted analysis of patients resuscitated from out-of-hospital VF/pVT arrest. In this observational study of 1721 patients, multivariate analysis found the prophylactic administration of lidocaine before hospitalization was associated with a significantly lower rate of recurrent VF/ pVT and higher rates of hospital admission and survival to hospital discharge. However, in a propensity score–adjusted analysis, rates of hospital admission and survival to hospital discharge did not differ between recipients of prophylactic lidocaine as compared with nonrecipients, although lidocaine was associated with less recurrent VF/pVT and there was no evidence of harm.190 Thus, evidence supporting a role for prophylactic lidocaine after VF/pVT arrest is weak at best, and nonexistent for cardiac arrest initiated by other rhythms.
Recommendations - Updated

There is insufficient evidence to support or refute the routine use of a β-blocker early (within the first hour) after ROSC.

(Class IIb, LOE C-LD)

There is insufficient evidence to support or refute the routine use of lidocaine early (within the first hour) after ROSC.

In the absence of contraindications, the prophylactic use of lidocaine may be considered in specific circumstances (such as during emergency medical services transport) when treatment of recurrent VF/pVT might prove to be challenging.

(Class IIb, LOE C-LD)

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

There is insufficient evidence to recommend for or against the routine initiation or continuation of other antiarrhythmic medications after ROSC from cardiac arrest.

Vasopressors in Cardiac Arrest - Updated

The 2015 ILCOR systematic review addresses the use of the vasopressors epinephrine and vasopressin during cardiac arrest. The new recommendations in this 2015 Guidelines Update apply only to the use of these vasopressors for this purpose.

In 2010 it was noted that, no placebo-controlled trials have shown that administration of any vasopressor agent at any stage during management of VF, pulseless VT, PEA, or asystole increases the rate of neurologically intact survival to hospital discharge. There is evidence, however, that the use of vasopressor agents is associated with an increased rate of ROSC.
Vasopressors in Cardiac Arrest: Standard-Dose Epinephrine - Updated

Epinephrine produces beneficial effects in patients during cardiac arrest, primarily because of its α-adrenergic (ie, vasoconstrictor) effects. These α-adrenergic effects of epinephrine can increase coronary perfusion pressure and cerebral perfusion pressure during CPR. The value and safety of the β-adrenergic effects of epinephrine are controversial because they may increase myocardial work and reduce subendocardial perfusion. The 2010 Guidelines stated that it is reasonable to consider administering a 1-mg dose of IV/IO epinephrine every 3 to 5 minutes during adult cardiac arrest.
2015 Evidence Summary

One trial191 assessed short-term and longer-term outcomes when comparing standard-dose epinephrine to placebo.  Standard-dose epinephrine was defined as 1 mg given IV/ IO every 3 to 5 minutes. For both survival to discharge and survival to discharge with good neurologic outcome, there was no benefit with standard-dose epinephrine; however, the study was stopped early and was therefore underpowered for analysis of either of these outcomes (enrolled approximately 500 patients as opposed to the target of 5000). There was, nevertheless, improved survival to hospital admission and improved ROSC with the use of standard-dose epinephrine. Observational studies were performed that evaluated epinephrine, with conflicting results.192,193
2015 Recommendation - Updated

Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest. (Class IIb, LOE B-R)
Vasopressors in Cardiac Arrest: Standard Dose Epinephrine Versus High-Dose Epinephrine - Updated

High doses of epinephrine are generally defined as doses in the range of 0.1 to 0.2 mg/kg. In theory, higher doses of epinephrine may increase coronary perfusion pressure, resulting in increased ROSC and survival from cardiac arrest. However, the adverse effects of higher doses of epinephrine in the postarrest period may negate potential advantages during the intraarrest period. Multiple case series followed by randomized trials have been performed to evaluate the potential benefit of higher doses of epinephrine. In the 2010 Guidelines, the use of high-dose epinephrine was not recommended except in special circumstances, such as for β-blocker overdose, calcium channel blocker overdose, or when titrated to real-time physiologically monitored parameters. In 2015, ILCOR evaluated the use of high-dose epinephrine compared with standard doses.
2015 Evidence Summary

A number of trials have compared outcomes from standard-dose epinephrine with those of high-dose epinephrine. These trials did not demonstrate any benefit for high-dose epinephrine over standard-dose epinephrine for survival to discharge with a good neurologic recovery (ie, Cerebral Performance Category score),194,195 survival to discharge,194-198 or survival to hospital admission.194-196,199 There was, however, a demonstrated ROSC advantage with highdose epinephrine.194-199
2015 Recommendation—New

High-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III: No Benefit, LOE B-R)
Vasopressors in Cardiac Arrest: Epinephrine Versus Vasopressin - Updated

Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary200,201 and renal vasoconstriction.202
2015 Evidence Summary

A single RCT203 enrolling 336 patients compared multiple doses of standard-dose epinephrine with multiple doses of standard dose vasopressin (40 units IV) in the emergency department after OHCA. The trial had a number of limitations but showed no benefit with the use of vasopressin for ROSC or survival to discharge with or without good neurologic outcome.
2015 Recommendation—Updated

Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest. (Class IIb, LOE B-R)

The removal of vasopressin has been noted in the Adult Cardiac Arrest Algorithm above (Figure 1).
Vasopressors in Cardiac Arrest: Epinephrine Versus Vasopressin in Combination With Epinephrine - Updated
2015 Evidence Summary

A number of trials have compared outcomes from standard dose epinephrine to those using the combination of epinephrine and vasopressin. These trials showed no benefit with the use of the epinephrine/vasopressin combination for survival to hospital discharge with Cerebral Performance Category score of 1 or 2 in 2402 patients,204-206 no benefit for survival to hospital discharge or hospital admission in 2438 patients,204-208 and no benefit for ROSC.204-209
2015 Recommendation—New

Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest. (Class IIb, LOE B-R)

The removal of vasopressin has been noted in the Adult Cardiac Arrest Algorithm above (Figure 1).
Vasopressors in Cardiac Arrest: Timing of Administration of Epinephrine - Updated
2015 Evidence Summary: IHCA

One large (n=25 905 patients) observational study of IHCA with nonshockable rhythms was identified,210 in which outcomes from early administration of epinephrine (1 to 3 minutes) were compared with outcomes from administration of epinephrine at 4 to 6 minutes, 7 to 9 minutes, and greater than 9 minutes. In this study, the early administration of epinephrine in nonshockable rhythms was associated with increased ROSC, survival to hospital discharge, and neurologically intact survival. No studies were identified specifically examining the effect of timing of administration of epinephrine after IHCA with shockable rhythms.
2015 Evidence Summary: OHCA

For nonshockable rhythms, 3 studies showed improved survival to hospital discharge with early administration of epinephrine. A study of 209 577 OHCA patients211 showed improved 1-month survival when outcomes from administration of epinephrine at less than 9 minutes of EMS-initiated CPR were compared with those in which epinephrine was administered at greater than 10 minutes. Another study enrolling 212 228 OHCA patients212 showed improved survival to discharge with early epinephrine (less than 10 minutes after EMS-initiated CPR) compared with no epinephrine. A smaller study of 686 OHCA patients213 showed improved rates of ROSC with early epinephrine (less than 10 minutes after 9-1-1 call) when the presenting rhythm was pulseless electrical activity. For shockable rhythms, there was no benefit with early administration of epinephrine, but there was a negative association of outcome with late administration. When neurologically intact survival to discharge was assessed,211,212,214 however, there was variable benefit with early administration of epinephrine for both shockable and nonshockable rhythms. Later administration of epinephrine was associated with a worse outcome. ROSC was generally improved with early administration of epinephrine in studies of more than 210 000 patients.198,211,213,215 Design flaws in the majority of these observational OHCA studies, however, included the use of a “no epinephrine” control arm as the comparator (thus not allowing for estimates on the effect of timing), and the lack of known timing of epinephrine administration upon arrival in the emergency department. In addition, the relationship of timing of defibrillation to timing of epinephrine is unknown for studies that included shockable rhythms.
2015 Recommendations—Updated

It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial non- shockable rhythm. (Class IIb, LOE C-LD)

There is insufficient evidence to make a recommendation as to the optimal timing of epinephrine, particularly in relation to defibrillation, when cardiac arrest is due to a shockable rhythm, because optimal timing may vary based on patient factors and resuscitation conditions.

Steroids - Updated

The use of steroids in cardiac arrest has been assessed in 2 clinical settings: IHCA and OHCA. In IHCA, steroids were combined with a vasopressor bundle or cocktail of epinephrine and vasopressin. Because the results of IHCA and OHCA were so different, these situations are discussed separately.
2015 Evidence Summary: IHCA

In an initial RCT involving 100 IHCA patients at a single center, the use of a combination of methylprednisolone, vasopressin, and epinephrine during cardiac arrest and hydrocortisone after ROSC for those with shock significantly improved survival to hospital discharge compared with the use of only epinephrine and placebo.216 In a subsequent 3-center study published in 2013,216 of 268 patients with IHCA (the majority coming from the same center as in the first study), the same combination of methylprednisolone, vasopressin, and epinephrine during cardiac arrest, and hydrocortisone for those with post-ROSC shock, significantly improved survival to discharge with good neurologic outcome compared with only epinephrine and placebo.

The same 2 RCTs provided evidence that the use of methylprednisolone and vasopressin in addition to epinephrine improved ROSC compared with the use of placebo and epinephrine alone.216,217
2015 Evidence Summary: OHCA

In OHCA, steroids have been evaluated in 1 RCT218 and 1 observational study.219 In these studies, steroids were not bundled as they were in the IHCA but studied as a sole treatment. When dexamethasone was given during cardiac arrest, it did not improve survival to hospital discharge or ROSC as compared with placebo.218 The observational study219 showed no benefit in survival to discharge but did show an association of improved ROSC with hydrocortisone compared with no hydrocortisone.
2015 Recommendations—New

There are no data to recommend for or against the routine use of steroids alone for IHCA patients.

In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post-arrest hydrocortisone as described by Mentzelopoulos et al 217 may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy.

  (Class IIb, LOE C-LD)

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

Access for Parenteral Medications During Cardiac Arrest

Timing of IV/IO Access

During cardiac arrest, provision of high-quality CPR and rapid defibrillation are of primary importance and drug administration is of secondary importance. After beginning CPR and attempting defibrillation for identified VF or pulseless VT, providers can establish IV or IO access. This should be performed without interrupting chest compressions. The primary purpose of IV/IO access during cardiac arrest is to provide drug therapy. Two clinical studies129,131 reported data suggesting worsened survival for every minute that antiarrhythmic drug delivery was delayed (measured from time of dispatch). However, this finding was potentially biased by a concomitant delay in onset of other ACLS interventions. In one study131 the interval from first shock to administration of an antiarrhythmic drug was a significant predictor of survival. One animal study220 reported lower CPP when delivery of a vasopressor was delayed. Time to drug administration was also a predictor of ROSC in a retrospective analysis of swine cardiac arrest.221 Thus, although time to drug treatment appears to have importance, there is insufficient evidence to specify exact time parameters or the precise sequence with which drugs should be administered during cardiac arrest.

Peripheral IV Drug Delivery

If a resuscitation drug is administered by a peripheral venous route, it should be administered by bolus injection and followed with a 20-mL bolus of IV fluid to facilitate the drug flow from the extremity into the central circulation.222 Briefly elevating the extremity during and after drug administration theoretically may also recruit the benefit of gravity to facilitate delivery to the central circulation but has not been systematically studied.

IO Drug Delivery

IO cannulation provides access to a noncollapsible venous plexus, enabling drug delivery similar to that achieved by peripheral venous access at comparable doses. Two prospective trials in children223 and adults224 and 6 other studies225-231 suggest that IO access can be established efficiently; is safe and effective for fluid resuscitation, drug delivery, and blood sampling for laboratory evaluation; and is attainable in all age groups. However, many of these studies were conducted during normal perfusion states or hypovolemic shock or in animal models of cardiac arrest. Although virtually all ACLS drugs have been given intraosseously in the clinical setting without known ill effects, there is little information on the efficacy and effectiveness of such administration in clinical cardiac arrest during ongoing CPR.

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

Commercially available kits can facilitate IO access in adults.

Central IV Drug Delivery

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

The primary advantage of a central line is that peak drug concentrations are higher and drug circulation times shorter compared with drugs administered through a peripheral IV catheter.232-234 In addition, a central line extending into the superior vena cava can be used to monitor ScvO2 and estimate CPP during CPR, both of which are predictive of ROSC.235,236 However, central line placement can interrupt CPR. Central venous catheterization is a relative (but not absolute) contraindication for fibrinolytic therapy in patients with acute coronary syndromes.

Endotracheal Drug Delivery

One study in children,237 5 studies in adults,238-242 and multiple animal studies243-245 have shown that lidocaine,239,246 epinephrine,247 atropine,248 naloxone, and vasopressin245 are absorbed via the trachea. There are no data regarding endotracheal administration of amiodarone. Administration of resuscitation drugs into the trachea results in lower blood concentrations than when the same dose is given intravascularly. Furthermore, the results of recent animal studies249,250 suggest that the lower epinephrine concentrations achieved when the drug is delivered endotracheally may produce transient β-adrenergic effects, resulting in vasodilation. These effects can be detrimental, causing hypotension, lower CPP and flow, and reduced potential for ROSC. Thus, although endotracheal administration of some resuscitation drugs is possible, IV or IO drug administration is preferred because it will provide more predictable drug delivery and pharmacologic effect.

In one nonrandomized cohort study of out-of-hospital cardiac arrest in adults251 using a randomized control, IV administration of atropine and epinephrine was associated with a higher rate of ROSC and survival to hospital admission than administration by the endotracheal route. Five percent of those who received IV drugs survived to hospital discharge, but no patient survived in the group receiving drugs by the endotracheal route.

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)

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. In 2 animal CPR studies the equipotent epinephrine dose given endotracheally was approximately 3 to 10 times higher than the IV dose.252,253 Providers should dilute the recommended dose in 5 to 10 mL of sterile water or normal saline and inject the drug directly into the endotracheal tube.247 Studies with epinephrine254 and lidocaine242 showed that dilution with sterile water instead of 0.9% saline may achieve better drug absorption.

Prognostication During CPR:End-Tidal CO2 - Updated

The 2015 ILCOR systematic review considered one intraarrest modality, ETCO2 measurement, in prognosticating outcome from cardiac arrest. This section focuses on whether a specific ETCO2 threshold can reliably predict ROSC and survival or inform a decision to terminate resuscitation efforts. The potential value of using ETCO2 as a physiologic monitor to optimize resuscitation efforts is discussed elsewhere (See Monitoring Physiologic Parameters During CPR, earlier in this Part).

ETCO2 is the partial pressure of exhaled carbon dioxide at the end of expiration and is determined by CO2 production, alveolar ventilation, and pulmonary blood flow. It is most reliably measured using waveform capnography, where the visualization of the actual CO2 waveform during ventilation ensures accuracy of the measurement. During low-flow states with relatively fixed minute ventilation, pulmonary blood flow is the primary determinant of ETCO2 . During cardiac arrest, ETCO2 levels reflect the cardiac output generated by chest compression. Low ETCO2 values may reflect inadequate cardiac output, but ETCO2 levels can also be low as a result of bronchospasm, mucous plugging of the ETT, kinking of the ETT, alveolar fluid in the ETT, hyperventilation, sampling of an SGA, or an airway with an air leak. It is particularly important to recognize that all of the prognostication studies reviewed in this section included only intubated patients. In nonintubated patients (those with bag-mask ventilation or SGA), ETCO2 may not consistently reflect the true value, making the measurement less reliable as a prognostication tool.

2015 Evidence Summary

Studies on the predictive capacity of ETCO2 among intubated patients during cardiac arrest resuscitation are observational, and none have investigated survival with intact neurologic outcome. An ETCO2 less than 10 mmHg immediately after intubation and 20 minutes after the initial resuscitation is associated with extremely poor chances for ROSC and survival.5,9,12,15,255

A prospective observational study of 127 IHCA patients found that an ETCO2 less than 10 mmHg at any point during the resuscitation was predictive of mortality, and only 1 patient with an ETCO2 value less than 10 mmHg survived to discharge.255 In that same study, an ETCO2 greater than 20 mmHg after 20 minutes of resuscitation was associated with improved survival to discharge.255 Another prospective observational study of 150 OHCA patients reported no survival to hospital admission when the ETCO2 was less than 10 mmHg after 20 minutes of resuscitation.5 Although these results suggest that ETCO2 can be a valuable tool to predict futility during CPR, potential confounding reasons for a low ETCO2 as listed above and the relatively small numbers of patients in these studies suggest that the ETCO2 should not be used alone as an indication to terminate resuscitative efforts. However, the failure to achieve an ETCO2 greater than 10 mmHg despite optimized resuscitation efforts may be a valuable component of a multimodal approach to deciding when to terminate resuscitation.

There are no studies that assess the prognostic value of ETCO2 measurements sampled from an SGA or bag-mask airway in predicting outcomes from a cardiac arrest.

2015 Recommendations—New

In intubated patients, failure to achieve an ETCO2 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)

The above recommendation is made with respect to ETCO2 in patients who are intubated, because the studies examined included only those who were intubated.

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)

Overview of Extracorporeal CPR - Updated

The 2015 ILCOR systematic review compared the use of ECPR (or ECMO) techniques for adult patients with IHCA and OHCA to conventional (manual or mechanical) CPR, in regard to ROSC, survival, and good neurologic outcome. The recommendations in this update apply only to the use of ECPR in this context.

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. The use of ECPR may allow providers additional time to treat reversible underlying causes of cardiac arrest (eg, acute coronary artery occlusion, pulmonary embolism, refractory VF, profound hypothermia, cardiac injury, myocarditis, cardiomyopathy, congestive heart failure, drug intoxication etc) or serve as a bridge for left ventricular assist device implantation or cardiac transplantation.

2015 Evidence Summary

All of the literature reviewed in the 2015 ILCOR systematic review comparing ECPR to conventional CPR was in the form of reviews, case reports, and observational studies. The low-quality evidence suggests a benefit in regard to survival and favorable neurologic outcome with the use of ECPR when compared with conventional CPR. There are currently no data from RCTs to support the use of ECPR for cardiac arrest in any setting.

One propensity-matched prospective observational study enrolling 172 patients with IHCA reported greater likelihood of ROSC and improved survival at hospital discharge, 30-day follow-up, and 1-year follow-up with the use of ECPR among patients who received more than 10 minutes of CPR. However, this study showed no difference in neurologic outcomes.256

A single retrospective, observational study enrolling 120 patients with witnessed IHCA who underwent more than 10 minutes of CPR reported a modest benefit over historic controls with the use of ECPR over continued conventional CPR in both survival and neurologic outcome at discharge and 6-month follow-up.257

A single propensity-matched, retrospective, observational study enrolling 118 patients with IHCA who underwent more than 10 minutes of CPR and then ECPR after cardiac arrest of cardiac origin showed no survival or neurologic benefit over conventional CPR at the time of hospital discharge, 30-day follow-up, or 1-year follow-up.258

One post hoc analysis of data from a prospective, observational cohort of 162 patients with OHCA who did not achieve ROSC with more than 20 minutes of conventional CPR, including propensity score matching, showed that ECPR was associated with a higher rate of neurologically intact survival than continued conventional CPR at 3-month follow-up.259

A single prospective, observational study enrolling 454 patients with OHCA who were treated with ECPR if they did not achieve ROSC with more than 15 minutes of conventional CPR after hospital arrival demonstrated improved neurologic outcomes at 1-month and 6-month follow-up.260

The key articles reviewed in the 2015 ILCOR systematic review comparing ECPR to conventional CPR feature some variability in their inclusion and exclusion criteria (Table 2), which may affect the generalizability of their results and could explain some of the inconsistencies in outcomes between studies.

Table 2: 2015 - Inclusion and Exclusion Criteria for Key Extracorporeal CPR Articles

2015 Recommendation—New

There is insufficient evidence to recommend the routine use of ECPR for patients with cardiac arrest. In settings where it can be rapidly implemented, ECPR may be considered for select cardiac arrest patients for whom the suspected etiology of the cardiac arrest is potentially reversible during a limited period of mechanical cardiorespiratory support. (Class IIb, LOE C-LD)

Interventions Not Recommended for Routine Use During Cardiac Arrest


Atropine sulfate reverses cholinergic-mediated decreases in heart rate and atrioventricular nodal conduction. No prospective controlled clinical trials have examined the use of atropine in asystole or bradycardic PEA cardiac arrest. Lower-level clinical studies provide conflicting evidence of the benefit of routine use of atropine in cardiac arrest.76,261-270 There is no evidence that atropine has detrimental effects during bradycardic or asystolic cardiac arrest.

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

Sodium Bicarbonate

Tissue acidosis and resulting acidemia during cardiac arrest and resuscitation are dynamic processes resulting from no blood flow during arrest and low blood flow during CPR. These processes are affected by the duration of cardiac arrest, level of blood flow, and arterial oxygen content during CPR. Restoration of oxygen content with appropriate ventilation with oxygen, support of some tissue perfusion and some cardiac output with high-quality chest compressions, then rapid ROSC are the mainstays of restoring acid-base balance during cardiac arrest.

Two studies demonstrated 271,272 increased ROSC, hospital admission, and survival to hospital discharge associated with use of bicarbonate. However, the majority of studies showed no benefit 273-275 or found a relationship with poor outcome.270,276-278

There are few data to support therapy with buffers during cardiac arrest. There is no evidence that bicarbonate improves the likelihood of defibrillation or survival rates in animals with VF cardiac arrest. A wide variety of adverse effects have been linked to administration of bicarbonate during cardiac arrest. Bicarbonate may compromise CPP by reducing systemic vascular resistance.279 It can create extracellular alkalosis that will shift the oxyhemoglobin saturation curve and inhibit oxygen release. It can produce hypernatremia and therefore hyperosmolarity. It produces excess CO2, which freely diffuses into myocardial and cerebral cells and may paradoxically contribute to intracellular acidosis.280 It can exacerbate central venous acidosis and may inactivate simultaneously administered catecholamines.

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

However, routine use of sodium bicarbonate is not recommended for patients in cardiac arrest. (Class III, LOE B)

When bicarbonate is used for special situations, an initial dose of 1 mEq/kg is typical. 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, providers should not attempt complete correction of the calculated base deficit. Other non–CO2-generating buffers such as carbicarb, THAM, or tribonate have shown potential for minimizing some adverse effects of sodium bicarbonate, including CO2 generation, hyperosmolarity, hypernatremia, hypoglycemia, intracellular acidosis, myocardial acidosis, and “overshoot” alkalosis.281-283 But clinical experience is greatly limited and outcome studies are lacking.


Studies of calcium during cardiac arrest have found variable results on ROSC, and no trial has found a beneficial effect on survival either in or out of hospital.267,270,284-289

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


Fibrinolytic therapy was proposed for use during cardiac arrest to treat both coronary thrombosis (acute coronary syndrome) with presumably complete occlusion of a proximal coronary artery and major life-threatening pulmonary embolism. Ongoing CPR is not an absolute contraindication to fibrinolysis. Initial studies were promising 290-296 and suggested benefit from fibrinolytic therapy in the treatment of victims of cardiopulmonary arrest unresponsive to standard therapy. But 2 large clinical trials 177,297 failed to show any improvement in outcome with fibrinolytic therapy during CPR. One of these showed an increased risk of intracranial bleeding associated with the routine use of fibrinolytics during cardiac arrest.177

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

IV Fluids

No published human study directly compares the outcome of routine IV fluid administration to no fluid administration during CPR. Most human and animal studies of fluid infusion during CPR did not have a control group,298-309 and 2 animal studies showed that normothermic fluid infusion during CPR caused a decrease in CPP.310-312 In addition to normothermic fluid, hypertonic and chilled fluids have been studied in animal and small human studies without a survival benefit.298,300,302-304,307-309 If cardiac arrest is associated with extreme volume losses, hypovolemic arrest should be suspected. These patients present with signs of circulatory shock advancing to PEA. In these settings intravascular volume should be promptly restored.


Electric pacing is generally not effective in cardiac arrest, and no studies have observed a survival benefit from pacing in cardiac arrest.313-316 Existing evidence suggests that pacing by transcutaneous, transvenous, or transmyocardial means in cardiac arrest does not improve the likelihood of ROSC or survival outcome regardless of the timing of pacing administration (early or delayed in established asystole), location of arrest (in-hospital or out-of-hospital), or primary cardiac rhythm (asystole, PEA) targeted for treatment.

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

Precordial Thump

The potential utility of precordial thump in cardiac arrest has not been well studied. When hemodynamically unstable ventricular tachyarrhythmias were induced during electrophysiological testing, initial administration of a precordial thump appeared to be safe but rarely effective in terminating ventricular arrhythmias.317 In a prospective observational study of patients with out-of-hospital cardiac arrest, precordial thump was associated with ROSC when administered promptly to patients with responder-witnessed asystolic arrest. When administered for VF/VT or PEA arrest it was ineffective but resulted in no apparent harm.318 In 3 case series319-321 VF or pulseless VT was converted to a perfusing rhythm by a precordial thump. Conversely, other case series documented deterioration in cardiac rhythm, such as rate acceleration of VT, conversion of VT to VF, or development of complete AV block or asystole following the thump.320,322-327

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.

There is insufficient evidence to recommend for or against the use of the precordial thump for witnessed onset of asystole, and there is insufficient evidence to recommend percussion pacing during typical attempted resuscitation from cardiac arrest.

When Should Resuscitative Efforts Stop?

The final decision to stop can never rest on a single parameter, such as duration of resuscitative efforts. Rather, clinical judgment and respect for human dignity must enter into decision making. In the out-of-hospital setting, cessation of resuscitative efforts in adults should follow system-specific criteria under direct medical control. There are limited clinical data to guide this decision in neonatal and pediatric out-of-hospital or in-hospital cardiac arrest. A more detailed discussion is provided in Part 3: Ethical Issues.


Intervention to prevent cardiac arrest in critically ill patients is ideal. When cardiac arrest occurs, high-quality CPR is fundamental to the success of any subsequent ACLS intervention. During resuscitation healthcare providers must perform chest compressions of adequate rate and depth, allow complete recoil of the chest after each compression, minimize interruptions in chest compressions, and avoid excessive ventilation, especially with an advanced airway. Quality of CPR should be continuously monitored. Physiologic monitoring may prove useful to optimize resuscitative efforts. For patients in VF/pulseless VT, shocks should be delivered promptly with minimal interruptions in chest compressions. The increased rates of ROSC associated with ACLS drug therapy have yet to be translated into long-term survival benefits. However, improved quality of CPR, advances in post–cardiac arrest care, and improved overall implementation through comprehensive systems of care may provide a pathway to optimize the outcomes of cardiac arrest patients treated with ACLS interventions.

Management of Symptomatic Bradycardia and Tachycardia


This section highlights recommendations for management of patients with acute symptomatic arrhythmias. 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 advanced cardiovascular life support (ACLS) providers base treatment decisions solely on rhythm interpretation and neglect clinical evaluation. Providers must evaluate the patient’s symptoms and clinical signs, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, and signs of inadequate organ perfusion.

Unstable and symptomatic are terms typically used to describe the condition of patients with arrhythmias. Generally, unstable refers to a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. Symptomatic implies that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases the provider must make an assessment as to whether it is the arrhythmia that is causing the patient to be unstable or symptomatic. For example, a patient in septic shock with sinus tachycardia of 140 beats per minute is unstable; however, the arrhythmia is a physiologic compensation rather than the cause of instability. Therefore, electric cardioversion will not improve this patient’s condition. Additionally, if a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient’s condition. 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.

The 2010 AHA Guidlines for CPR and ECC emphasize the importance of clinical evaluation and highlight principles of therapy with algorithms that have been refined and streamlined since publication of the 2005 AHA Guidelines for CPR and ECC.328 The key principles of arrhythmia recognition and management in adults are as follows:

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)

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.

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

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)

If the patient with tachycardia is stable, determine if the patient has a narrow-complex or wide-complex tachycardia, whether the rhythm is regular or irregular, and for wide complexes whether the QRS morphology is monomorphic or polymorphic. Therapy is then tailored accordingly (Table 3).

Table 3: 2010 - IV Drugs Used for Tachycardia

Know when to call for expert consultation regarding complicated rhythm interpretation, drugs, or management decisions.

A comprehensive presentation of the evaluation and management of bradyarrhythmias and tachyarrhythmias is beyond the scope of this document. The following selected rhythm scenarios are meant to aid with the management of periarrest rhythm disorders. If cardiac arrest develops at any time, see the ACLS Cardiac Arrest Algorithms above (Figure 1,Figure 2).


This section summarizes the management of bradyarrhythmias. Following the overview of bradyarrhythmias and summary of the initial evaluation and treatment of bradycardia, drugs used in the treatment of bradycardia are presented. See the Bradycardia Algorithm, Figure 3. Box numbers in the text refer to the numbered boxes in the algorithm.

Figure 3: Adult Bradycardia With a Pulse Algorithm

Bradycardia is defined as a heart rate of <60 beats per minute. However, when bradycardia is the cause of symptoms, the rate is generally <50 beats per minute, which is the working definition of bradycardia used here (Figure 3: Bradycardia Algorithm, Box 1). A slow heart rate may be physiologically normal for some patients, whereas a heart rate of >50 beats per minut1e may be inadequate for others. The Bradycardia Algorithm focuses on management of clinically significant bradycardia (ie, bradycardia that is inappropriate for the clinical condition).

Because hypoxemia is a common cause of bradycardia, initial evaluation of any patient with bradycardia should focus 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.

The provider must 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, the provider should reassess the underlying cause of the patient’s symptoms. Remember that 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, the patient should receive immediate treatment.

Atrioventricular (AV) blocks are classified as first-, second-, and third-degree. Blocks may be caused by medications or electrolyte disturbances, as well as structural problems resulting from AMI or other myocardial diseases. A first-degree AV block is defined by a prolonged PR interval (>0.20 second) and is generally benign. Second-degree AV block is divided into Mobitz types I and II. In Mobitz type I block, the block is at the AV node; the block is often transient and asymptomatic. In Mobitz type II block, the block is usually below the AV node within the His-Purkinje system; this block is often symptomatic, with the potential to progress to complete (third-degree) AV block. Third-degree AV block may occur at the AV node, bundle of His, or bundle branches. When third-degree AV block is present, no impulses pass between the atria and ventricles. Third-degree AV block can be permanent or transient, depending on the underlying cause.
Therapy (Figure 3 Box 5)

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

Clinical trials in adults329-333 showed that IV atropine improved heart rate, symptoms, and signs associated with bradycardia. Atropine sulfate reverses cholinergic-mediated decreases in heart rate and should be considered a temporizing measure while awaiting a transcutaneous or transvenous pacemaker for patients with symptomatic sinus bradycardia, conduction block at the level of the AV node, or sinus arrest.333

The recommended atropine dose for bradycardia is 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.334 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. One small uncontrolled study documented paradoxical slowing of the heart rate and high-degree AV block when atropine was administered to patients after cardiac transplantation.335

Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block 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 TCP or β-adrenergic support as temporizing measures while the patient is prepared for transvenous pacing (Figure 3, Box 6).

TCP may be useful for the treatment of symptomatic bradycardias. There are limited studies comparing TCP with drug therapy for the treatment of symptomatic bradycardia. A randomized controlled trial in which atropine and glycopyrrolate were compared with TCP showed few differences in outcome and survival, although the TCP group obtained a more consistent heart rate.329 In a study evaluating the feasibility of treatment with dopamine as compared with TCP, no differences were observed between treatment groups in survival to hospital discharge.336  TCP is, at best, a temporizing measure. TCP is painful in conscious patients, and, whether effective or not (achieving inconsistent capture), the patient should be prepared for transvenous pacing and expert consultation should be obtained.

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

Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. (Class IIb, LOE C)

If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated (Figure 3, Box 6). (Class IIa, LOE C)
Alternative Drugs to Consider

Although not first-line agents for treatment of symptomatic bradycardia, dopamine, epinephrine, and isoproterenol are alternatives when a bradyarrhythmia is unresponsive to or inappropriate for treatment with atropine, or as a temporizing measure while awaiting the availability of a pacemaker. Alternative drugs may also be appropriate in special circumstances such as the overdose of a β-blocker or calcium channel blocker.

Dopamine hydrochloride is a catecholamine with both α- and β-adrenergic actions. It can be titrated to more selectively target heart rate or vasoconstriction. At lower doses dopamine has a more selective effect on inotropy and heart rate; at higher doses (>10 mcg/kg per minute), it also has vasoconstrictive effects.

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)

Begin dopamine infusion at 2 to 10 mcg/kg per minute and titrate to patient response.336 Use of vasoconstrictors requires that the recipient be assessed for adequate intravascular volume and volume status supported as needed.

Epinephrine is a catecholamine with α- and β-adrenergic actions.

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)

Begin the infusion at 2 to 10 mcg/min and titrate to patient response. Use of vasoconstrictors requires that the recipient be assessed for adequate intravascular volume and volume status supported as needed.

Isoproterenol is a β-adrenergic agent with β-1 and β-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.


This section summarizes the management of a wide variety of tachyarrhythmias. Following the overview of tachyarrhythmias and summary of the initial evaluation and treatment of tachycardia, common antiarrhythmic drugs used in the treatment of tachycardia are presented. See the Tachycardia Algorithm, Figure 4. Box numbers in the text refer to the numbered boxes in the algorithm.

Figure 4: Adult Tachycardia With a Pulse Algorithm

Classification of Tachyarrhythmias

Tachycardias can be classified in several ways, based on the appearance of the QRS complex, heart rate, and regularity. ACLS professionals should be able to recognize and differentiate between sinus tachycardia, narrow-complex supraventricular tachycardia (SVT), and wide-complex tachycardia. Because ACLS providers may be unable to distinguish between supraventricular and ventricular rhythms, they should be aware that most wide-complex (broad-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 (MAT)

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

Irregular narrow-complex tachycardias are likely atrial fibrillation or MAT; occasionally atrial flutter is irregular. The management of atrial fibrillation and flutter is discussed in the section “Irregular Tachycardias” below.

Initial Evaluation and Treatment of Tachyarrhythmias

Tachycardia is defined as an arrhythmia with a rate of >100 beats per minute, although, as with defining bradycardia, the rate of a tachycardia takes on clinical significance at its greater extremes and is more likely attributable to an arrhythmia rate of ≥150 beats per minute (Figure 4: Tachycardia Algorithm, Box 1). A rapid heart rate is an appropriate response to a physiologic stress (eg, fever, dehydration) or other underlying conditions. When encountering patients with tachycardia, efforts should be made 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. Many experts suggest that 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.

The evaluation and management of tachyarrhythmias is depicted in the ACLS Tachycardia With Pulse Algorithm (Figure 4: Tachycardia Algorithm). Box numbers in the text refer to numbered boxes in this algorithm. If cardiac arrest develops at any time, see the ACLS Cardiac Arrest Algorithms in this document above under 4.1: “Management of Cardiac Arrest.”

Because hypoxemia is a common cause of tachycardia, initial evaluation of any patient with tachycardia should focus 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 available, obtain a 12-lead ECG to better define the rhythm, but this should 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, the provider should 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). However, with ventricular rates <150 beats per minute in the absence of ventricular dysfunction, it is more likely that the tachycardia is secondary to the underlying condition rather than the 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)

If the patient with tachycardia is stable (ie, no serious signs related to the tachycardia), the provider has time to obtain a 12-lead ECG, evaluate the rhythm, determine if the width of the QRS complex is ≥0.12 second (Box 5), and determine treatment options. Stable patients may await expert consultation because treatment has the potential for harm.


If possible, establish IV access before cardioversion and administer sedation if the patient is conscious. Do not delay cardioversion if the patient is extremely unstable.
Synchronized Cardioversion and Unsynchronized Shocks

Refer to Figure 4: Tachycardia Algorithm – Box 4.

Synchronized cardioversion is shock delivery that is timed (synchronized) with the QRS complex. This synchronization avoids shock delivery during the relative refractory period of the cardiac cycle when a shock could produce VF.337 If cardioversion is needed and it is impossible to synchronize a shock, use high-energy unsynchronized shocks (defibrillation doses).

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 these tachyarrhythmias by interrupting the underlying reentrant pathway that is responsible for them.
Waveform and Energy

The recommended initial biphasic energy dose for cardioversion of atrial fibrillation is 120 to 200 J.338-342 (Class IIa, LOE A)

If the initial shock fails, providers should increase the dose in a stepwise fashion.

Cardioversion of atrial flutter and other SVTs generally requires less energy; an initial energy of 50 J to 100 J is often sufficient.342 If the initial 50-J shock fails, the provider should increase the dose in a stepwise fashion.343

Cardioversion of atrial fabrillation with monophasic waveforms should begin at 200 J and increase in stepwise fashion if not successful.338-340 (Class IIa, LOE B)

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. No studies were identified that addressed this issue. Thus, this recommendation represents expert opinion. (Class IIb, LOE C)

Arrhythmias with a polymorphic QRS appearance (such as torsades de pointes) will usually not permit synchronization. Thus, if a patient has polymorphic VT, treat the rhythm as VF and deliver high-energy unsynchronized shocks (ie, defibrillation doses). 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). Use the ACLS Cardiac Arrest Algorithms in this document above under 4.1: “Management of Cardiac Arrest.”

Regular Narrow-Complex Tachycardia
Sinus Tachycardia

Sinus tachycardia is common and usually results from a physiologic stimulus, such as fever, anemia, or hypotension/shock. Sinus tachycardia is defined as a heart rate >100 beats per minute. The upper rate of sinus tachycardia is age-related (calculated as approximately 220 beats 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. If judged to be sinus tachycardia, no specific drug treatment is required. Instead, therapy is directed toward identification and treatment of the underlying cause. When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In such compensatory tachycardias, stroke volume is limited, so “normalizing” the heart rate can be detrimental.
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 (<120 milliseconds or <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 reentry circuit may also reside in whole or in part in the AV node itself. This results in AV nodal reentry tachycardia (AVNRT) if both limbs of the reentry circuit involve AV nodal tissue. Alternatively, it may result in AV reentry tachycardia (AVRT) if one limb of the reentry circuit involves an accessory pathway and the other involves the AV node. The characteristic abrupt onset and termination of each of the latter groups of reentrant tachyarrhythmias (AVNRT and AVRT) led to the original name, paroxysmal supraventricular tachycardia (PSVT). This subgroup of reentry arrhythmias, due to either AVNRT or AVRT, is characterized by abrupt onset and termination and a regular rate that exceeds the typical upper limits of sinus tachycardia at rest (usually >150 beats per minute) and, in the case of an AVNRT, often presents without readily identifiable P waves on the ECG.

Distinguishing the forms of reentrant SVTs that are based in atrial myocardium (such as atrial fibrillation) versus those with a reentry circuit partly or wholly based in the AV node itself (PSVT) is important because each will respond differently to therapies aimed at impeding conduction through the AV node. 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. Conversely, reentry arrhythmias for which at least one limb of the circuit resides in the AV node (PSVT attributable to AVNRT or AVRT) can be terminated by such drugs.

Yet another group of SVTs is referred to as automatic tachycardias. These arrhythmias are not due to a circulating circuit but to an excited automatic focus. Unlike the abrupt pattern of reentry, the characteristic onset and termination of these tachyarrhythmias are more gradual and analogous to how the sinus node behaves in gradually accelerating and slowing heart rate. These automatic arrhythmias include ectopic atrial tachycardia, MAT, and junctional tachycardia. These 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.
Vagal Maneuvers

Vagal maneuvers and adenosine are the preferred initial therapeutic choices for the termination of stable PSVT (Figure 4: Tachycardia Algorithm, Box 7). Vagal maneuvers alone (Valsalva maneuver or carotid sinus massage) will terminate up to 25% of PSVTs.344-346 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.

If PSVT does not respond to vagal maneuvers, give 6 mg of IV adenosine as a rapid IV push through a large (eg, antecubital) vein followed by a 20 mL saline flush. (Class I, LOE B)

If the rhythm does not convert within 1 to 2 minutes, give a 12 mg rapid IV push using the method above. Because of 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. As with vagal maneuvers, the effect of adenosine on other SVTs (such as atrial fibrillation or flutter) is to transiently slow ventricular rate (which may be useful diagnostically) but not afford their termination or meaningful lasting rate control.

A number of studies347-364 support the use of adenosine in the treatment of stable PSVT. Although 2 randomized clinical trials349,352 documented a similar PSVT conversion rate between adenosine and calcium channel blockers, adenosine was more rapid and had fewer severe side effects than verapamil. Amiodarone as well as other antiarrhythmic agents can be useful in the termination of PSVT, but the onset of action of amiodarone is slower than that of adenosine,365 and the potential proarrhythmic risks of these agents favor the use of safer treatment alternatives.

Adenosine is safe and effective in pregnancy.366 However, adenosine does have several important drug interactions. Larger doses may be required for patients with a significant blood level of theophylline, caffeine, or theobromine. The initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine, those with transplanted hearts, or if given by central venous access. Side effects with adenosine are common but transient; flushing, dyspnea, and chest discomfort are the most frequently observed.367 Adenosine should not be given to patients with asthma.

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.
Calcium Channel Blockers and β-Blockers

If adenosine or vagal maneuvers fail to convert PSVT, PSVT 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 β-blockers. (Class IIa, LOE C)

These drugs act primarily on nodal tissue either to terminate the reentry PSVTs that depend on conduction through the AV node or to slow the ventricular response to other SVTs by blocking conduction through the AV node. The alternate mechanism of action and longer duration of these drugs may result in more sustained termination of PSVT or afford more sustained rate control of atrial arrhythmias (such as atrial fibrillation or flutter). A number of studies have established the effectiveness of verapamil347,349,350,352,360, 364,368-371 and diltiazem368,372,373 in converting PSVT to normal sinus rhythm.

For verapamil, give a 2.5 mg to 5 mg IV bolus over 2 minutes (over 3 minutes in older patients). If there is no therapeutic response and no drug-induced adverse event, repeated doses of 5 mg to 10 mg may be administered every 15 to 30 minutes to a total dose of 20 mg. An alternative dosing regimen is to give a 5 mg bolus every 15 minutes to a total dose of 30 mg. Verapamil should be given only to patients with narrow-complex reentry SVT or arrhythmias known with certainty to be of supraventricular origin. Verapamil should not be given to patients with wide-complex tachycardias. It should not be given to patients with impaired ventricular function or heart failure.

For diltiazem, give a dose of 15 mg to 20 mg (0.25 mg/kg) IV over 2 minutes; if needed, in 15 minutes give an additional IV dose of 20 mg to 25 mg (0.35 mg/kg). The maintenance infusion dose is 5 mg/hour to 15 mg/hour, titrated to heart rate.

A wide variety of IV β-blockers are available for treatment of supraventricular tachyarrhythmias. These include metoprolol, atenolol, propranolol, esmolol, and labetolol (the latter more commonly used for acute management of hypertension than for arrhythmias). In principle these agents exert their effect by antagonizing sympathetic tone in nodal tissue, resulting in slowing of conduction. Like calcium channel blockers, they also have negative inotropic effects and further reduce cardiac output in patients with heart failure. More detailed information is provided below. Side effects of β-blockers can include bradycardias, AV conduction delays, and hypotension. β-blockers should be used with caution in patients with obstructive pulmonary disease or congestive heart failure.

Caution is advised 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, β-blockers, or digoxin) is unlikely to slow the ventricular rate and in some instances may accelerate the ventricular response.

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

Caution is also advised to avoid the combination of AV nodal blocking agents that have a longer duration of action. For example, the short elimination half-life of adenosine affords follow-up treatment, if required, with a calcium channel blocker or β-blocker. Conversely the longer half-life of a calcium channel or β-blocker means their effects will overlap; profound bradycardia can develop if they are given serially.

Although antiarrhythmic medications (eg, amiodarone, procainamide, or sotalol) can also be used to treat SVTs, the higher toxicity and risk for proarrhythmia make these medications less desirable alternatives to the described AV nodal blocking agents. A possible exception is in patients with pre-excited atrial arrhythmias; the typical AV nodal blocking drugs are contraindicated in these patients and rate control may be achieved with antiarrhythmic medications. Importantly, use of these agents for atrial-based SVTs, such as atrial fibrillation and flutter can result in their termination, which may be undesirable in the absence of precautions to prevent the thromboembolic complications that may result from such conversion.

Wide-Complex Tachycardia

The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Figure 4: Tachycardia Algorithm, Box 3). An unstable patient with a wide-complex tachycardia should be presumed to have VT and immediate cardioversion should be performed (Box 4 and see above).

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)

If the patient is stable, the second step in management is to obtain a 12-lead ECG (Boxes 6 and 7) to evaluate the rhythm. At this point the provider should consider the need to obtain expert consultation. If the patient becomes unstable at any time, proceed with synchronized cardioversion or unsynchronized defibrillation should the arrhythmia deteriorate to VF or be due to a polymorphic VT.

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

The third step in management of a tachycardia is to determine if the rhythm is regular or irregular. A regular wide-complex tachycardia is likely to be VT or SVT with aberrancy. An irregular wide-complex tachycardia may be atrial fibrillation with aberrancy, pre-excited atrial fibrillation (ie, atrial fibrillation using an accessory pathway for antegrade conduction), or polymorphic VT/torsades de pointes. Providers should consider the need for expert consultation when treating wide-complex tachycardias.
Therapy for Regular Wide-Complex Tachycardias

In patients with stable undifferentiated wide-QRS complex tachycardia, a reasonable approach is to try to identify the wide-complex tachycardia as SVT or VT and treat based on the algorithm for that rhythm.

If the etiology of the rhythm cannot be determined, the rate is regular, and the QRS is monomorphic, recent evidence suggests that IV adenosine is relatively safe for both treatment and diagnosis.374 (Class IIb, LOE B)

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

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 due to 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. Because close attention to these varying responses may help to diagnose the underlying rhythm, whenever possible, continuous ECG recording is strongly encouraged to provide such written documentation. This documentation can be invaluable in helping to establish a firm rhythm diagnosis 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.

Depending on the underlying rhythm, the response to adenosine challenge can be variable. Some studies375-379 showed that adenosine converted an undifferentiated wide-complex tachycardia to sinus rhythm. Another study380 showed poor rates of conversion to sinus rhythm in patients known to have VT. The following adverse effects were reported in patients with pre-excited atrial fibrillation treated with adenosine: conversion to atrial fibrillation with a rapid ventricular response in one patient later found to have preexcitation, conversion to VF in one patient with known WPW,381 conversion to VF in 4 patients with pre-excited atrial fibrillation,382 conversion to VF in 2 patients with WPW,383 and a single case of VF in a patient with VT.384

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

Adverse effects when the rhythm was due to VT were shown in 5 small case series.381-385 Profound hypotension was reported in 11 of 25 patients known to have VT treated with verapamil.385

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

If IV antiarrhythmics are administered, procainamide,(Class IIa, LOE B) amiodarone, or sotalol can be considered. (Class IIb, LOE B)

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)

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

One randomized comparison found procainamide (10 mg/kg) to be superior to lidocaine (1.5 mg/kg) for termination of hemodynamically stable monomorphic VT.386 Procainamide can be administered at a rate of 20 to 50 mg/min until the arrhythmia is suppressed, hypotension ensues, QRS duration increases >50%, or the maximum dose of 17 mg/kg is given. Maintenance infusion is 1 to 4 mg/min. Procainamide should be avoided in patients with prolonged QT and congestive heart failure.

IV sotalol (100 mg IV over 5 minutes) was found to be more effective than lidocaine (100 mg IV over 5 minutes) when administered to patients with spontaneous hemodynamically stable sustained monomorphic VT in a double-blind randomized trial within a hospital setting.387 In a separate study of 109 patients with a history of spontaneous and inducible sustained ventricular tachyarrhythmias, infusing 1.5 mg/kg of sotalol over ≤5 minutes was found to be relatively safe and effective, causing hypotension in only 2 patients, both of whom responded to IV fluid.388 Package insert recommends slow infusion, but the literature supports more rapid infusion of 1.5 mg/kg over 5 minutes or less. Sotalol should be avoided in patients with a prolonged QT interval.

Amiodarone is also effective in preventing recurrent monomorphic VT or treating refractory ventricular arrhythmias389,,390-392 in patients with coronary artery disease and poor ventricular function. It is given 150 mg IV over 10 minutes; dosing should be repeated as needed to a maximum dose of 2.2 g IV per 24 hours. Higher doses (300 mg) were associated with an increased frequency of hypotension, although some reports390,392 attributed the hypotension to the vasoactive solvents that are not present in a new form of the drug recently approved for use in the US.

By comparison, lidocaine is less effective in terminating VT than procainamide, sotalol, and amiodarone,389,386,387 and when given to patients with or without a history of MI with spontaneous sustained stable VT in the hospital setting.380,393,394 Lidocaine has been reported to variably terminate VT when administered intramuscularly to patients with AMI and VT in the out-of-hospital setting.395,396 Thus, while occasionally effective, lidocaine should be considered second-line antiarrhythmic therapy for monomorphic VT. Lidocaine can be administered at a dose of 1 to 1.5 mg/kg IV bolus. Maintenance infusion is 1 to 4 mg/min (30 to 50 mcg/kg per minute).

Irregular Tachycardias

Atrial Fibrillation and Flutter

An irregular narrow-complex or wide-complex tachycardia 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.

General management of atrial fibrillation should focus 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.397
Rate Control

Patients who are hemodynamically unstable should receive prompt electric cardioversion. More stable patients require ventricular rate control as directed by patient symptoms and hemodynamics.

IV β-blockers and nondihydropyridine calcium channel blockers such as diltiazem398-401 are the drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular response. (Class IIa, LOE A)

Digoxin402-404 and amiodarone405,406 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 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.
Rhythm Control

A variety of agents have been shown to be effective in terminating atrial fibrillation (pharmacologic or chemical cardioversion), although success between them varies and not all are available as parenteral formulations. Expert consultation is recommended.

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.

If a long QT interval is observed during sinus rhythm (ie, the VT is torsades de pointes), the first step is to stop medications known to prolong the QT interval. Correct electrolyte imbalance and other acute precipitants (eg, drug overdose or poisoning: see Part 12.7: “Cardiac Arrest Associated With Toxic Ingestions”). Although magnesium is commonly used to treat torsades de pointes VT (polymorphic VT associated with long QT interval), it is supported by only 2 observational studies407,408 that showed effectiveness in patients with prolonged QT interval. One adult case series409 showed that isoproterenol or ventricular pacing can be effective in terminating torsades de pointes associated with bradycardia and drug-induced QT prolongation. Polymorphic VT associated with familial long QT syndrome may be treated with IV magnesium, pacing, and/or β-blockers; isoproterenol should be avoided. Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. 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 β-blockers may reduce the frequency of arrhythmia recurrence. (Class IIb, LOE C)

Myocardial ischemia should be treated with β-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,407 but amiodarone may be effective.410 (Class IIb, LOE C)

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


The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

Authorship and Disclosures

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

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


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.

© Copyright 2015 American Heart Association, Inc.


  1. Spindelboeck W, Schindler O, Moser A, Hausler F, Wallner S, Strasser C, Haas J, Gemes G, Prause G. Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission. Resuscitation. 2013;84:770–775. doi: 10.1016/j. resuscitation.2013.01.012.
  2. Meaney PA, Bobrow BJ, Mancini ME, Christenson J, de Caen AR, Bhanji F, Abella BS, Kleinman ME, Edelson DP, Berg RA, Aufderheide TP, Menon V, Leary M; CPR Quality Summit Investigators, the American Heart Association Emergency Cardiovascular Care Committee, and the Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation. Cardiopulmonary resuscitation quality: [corrected] improv- ing cardiac resuscitation outcomes both inside and outside the hospital: a consensus statement from the American Heart Association. Circulation. 2013;128:417–435. doi: 10.1161/CIR.0b013e31829d8654.
  3. Halperin HR, Tsitlik JE, Gelfand M, Weisfeldt ML, Gruben KG, Levin HR, Rayburn BK, Chandra NC, Scott CJ, Kreps BJ. A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest. N Engl J Med. 1993;329:762–768. doi: 10.1056/NEJM199309093291104.
  4. Kern KB, Hilwig RW, Berg RA, Ewy GA. Efficacy of chest compres- sion-only BLS CPR in the presence of an occluded airway. Resuscitation. 1998;39:179–188.
  5. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997;337:301–306. doi: 10.1056/NEJM199707313370503.
  6. Lindner KH, Prengel AW, Pfenninger EG, Lindner IM, Strohmenger HU, Georgieff M, Lurie KG. Vasopressin improves vital organ blood flow during closed-chest cardiopulmonary resuscitation in pigs. Circulation. 1995;91:215–221.
  7. Little CM, Angelos MG, Paradis NA. Compared to angiotensin II, epi- nephrine is associated with high myocardial blood flow following return of spontaneous circulation after cardiac arrest. Resuscitation. 2003;59:353–359.
  8. Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M, Nowak RM. Coronary perfusion pressure and the return of sponta- neous circulation in human cardiopulmonary resuscitation. JAMA. 1990;263:1106–1113.
  9. Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon diox- ide to predict outcome in prehospital cardiac arrest. Ann Emerg Med. 1995;25:762–767.
  10. Bhende MS, Thompson AE. Evaluation of an end-tidal CO2 detector dur- ing pediatric cardiopulmonary resuscitation. Pediatrics. 1995;95:395–399.
  11. Ornato JP, Shipley JB, Racht EM, Slovis CM, Wrenn KD, Pepe PE, Almeida SL, Ginger VF, Fotre TV. Multicenter study of a portable, hand- size, colorimetric end-tidal carbon dioxide detection device. Ann Emerg Med. 1992;21:518–523.
  12. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resus- citation from end-tidal carbon dioxide concentration. Crit Care Med. 1990;18:358–362.
  13. Sanders AB, Ogle M, Ewy GA. Coronary perfusion pressure during cardio- pulmonary resuscitation. Am J Emerg Med. 1985;3:11–14.
  14. Rivers EP, Martin GB, Smithline H, Rady MY, Schultz CH, Goetting MG, Appleton TJ, Nowak RM. The clinical implications of continuous central venous oxygen saturation during human CPR. Ann Emerg Med. 1992;21:1094–1101.
  15. Cantineau JP, Lambert Y, Merckx P, Reynaud P, Porte F, Bertrand C, Duvaldestin P. End-tidal carbon dioxide during cardiopulmonary resusci- tation in humans presenting mostly with asystole: a predictor of outcome. Crit Care Med. 1996;24:791–796.
  16. Grmec S, Kupnik D. Does the Mainz Emergency Evaluation Scoring (MEES) in combination with capnometry (MEESc) help in the prognosis of outcome from cardiopulmonary resuscitation in a prehospital setting? Resuscitation. 2003;58:89–96.
  17. Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricu- lar tachycardia cardiac arrest in the prehospital setting. Crit Care. 2003;7:R139–R144. doi: 10.1186/cc2369.
  18. Grmec S, Klemen P. Does the end-tidal carbon dioxide (EtCO2) concen- tration have prognostic value during out-of-hospital cardiac arrest? Eur J Emerg Med. 2001;8:263–269.
  19. Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care. 2008;12:R115. doi: 10.1186/cc7009.
  20. Steedman DJ, Robertson CE. Measurement of end-tidal carbon dioxide concentration during cardiopulmonary resuscitation. Arch Emerg Med. 1990;7:129–134.
  21. Pokorná M, Necas E, Kratochvíl J, Skripský R, Andrlík M, Franek O. A sudden increase in partial pressure end-tidal carbon dioxide (P(ET) CO(2)) at the moment of return of spontaneous circulation. J Emerg Med. 2010;38:614–621. doi: 10.1016/j.jemermed.2009.04.064.
  22. Sehra R, Underwood K, Checchia P. End tidal CO2 is a quantitative mea- sure of cardiac arrest. Pacing Clin Electrophysiol. 2003;26(1 Pt 2):515–517.
  23. Grmec S, Krizmaric M, Mally S, Kozelj A, Spindler M, Lesnik B. Utstein style analysis of out-of-hospital cardiac arrest–bystander CPR and end expired carbon dioxide. Resuscitation. 2007;72:404–414. doi: 10.1016/j. resuscitation.2006.07.012.
  24. Entholzner E, Felber A, Mielke L, Hargasser S, Breinbauer B, Hundelshausen VB, Hipp R. Assessment of end-tidal CO2 measure- ment in reanimation. Anasthesiol Intensivmed Notfallmed Schmerzther. 1992;27:473–476.
  25. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal car- bon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987;257:512–515.
  26. Bhende MS, Karasic DG, Karasic RB. End-tidal carbon dioxide changes during cardiopulmonary resuscitation after experimental asphyxial cardiac arrest. Am J Emerg Med. 1996;14:349–350. doi: 10.1016/ S0735-6757(96)90046-7.
  27. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318:607–611. doi: 10.1056/NEJM198803103181005.
  28. Axelsson C, Karlsson T, Axelsson AB, Herlitz J. Mechanical active com- pression-decompression cardiopulmonary resuscitation (ACD-CPR) ver- sus manual CPR according to pressure of end tidal carbon dioxide (P(ET) CO2) during CPR in out-of-hospital cardiac arrest (OHCA). Resuscitation. 2009;80:1099–1103. doi: 10.1016/j.resuscitation.2009.08.006.
  29. Berryman CR, Phillips GM. Interposed abdominal compression-CPR in human subjects. Ann Emerg Med. 1984;13:226–229.
  30. Cha KC, Kim HJ, Shin HJ, Kim H, Lee KH, Hwang SO. Hemodynamic effect of external chest compressions at the lower end of the sternum in cardiac arrest patients. J Emerg Med. 2013;44:691–697. doi: 10.1016/j. jemermed.2012.09.026.
  31. Duchateau FX, Gueye P, Curac S, Tubach F, Broche C, Plaisance P, Payen D, Mantz J, Ricard-Hibon A. Effect of the AutoPulse automated band chest compression device on hemodynamics in out-of-hospital car- diac arrest resuscitation. Intensive Care Med. 2010;36:1256–1260. doi: 10.1007/s00134-010-1784-x.
  32. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW, Ewy GA. A study of chest compression rates during cardiopulmonary resuscitation in humans. The importance of rate-directed chest compressions. Arch Intern Med. 1992;152:145–149.
  33. Manning JE. Feasibility of blind aortic catheter placement in the pre- hospital environment to guide resuscitation in cardiac arrest. J Trauma Acute Care Surg. 2013;75(2 suppl 2):S173–S177. doi: 10.1097/ TA.0b013e318299d9ee.
  34. Orliaguet GA, Carli PA, Rozenberg A, Janniere D, Sauval P, Delpech P. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscita- tion: comparison of active compression-decompression and standard CPR. Ann Emerg Med. 1995;25:48–51.
  35. Plaisance P, Lurie KG, Payen D. Inspiratory impedance during active com- pression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest. Circulation. 2000;101:989–994.
  36. Segal N, Parquette B, Ziehr J, Yannopoulos D, Lindstrom D. Intrathoracic pressure regulation during cardiopulmonary resuscitation: a feasibility case-series. Resuscitation. 2013;84:450–453. doi: 10.1016/j. resuscitation.2012.07.036.
  37. Timerman S, Cardoso LF, Ramires JA, Halperin H. Improved hemody- namic performance with a novel chest compression device during treat- ment of in-hospital cardiac arrest. Resuscitation. 2004;61:273–280. doi: 10.1016/j.resuscitation.2004.01.025.
  38. Ward KR, Sullivan RJ, Zelenak RR, Summer WR. A comparison of inter- posed abdominal compression CPR and standard CPR by monitoring end- tidal PCO2. Ann Emerg Med. 1989;18:831–837.
  39. Ward KR, Menegazzi JJ, Zelenak RR, Sullivan RJ, McSwain NE Jr. A comparison of chest compressions between mechanical and manual CPR by monitoring end-tidal PCO2 during human cardiac arrest. Ann Emerg Med. 1993;22:669–674.
  40. Narasimhan M, Koenig SJ, Mayo PH. Advanced echocardiography for the critical care physician: part 1. Chest. 2014;145:129–134. doi: 10.1378/ chest.12-2441.
  41. Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management: concept of an advanced life support-conformed algorithm. Crit Care Med. 2007;35(5 suppl):S150–S161. doi: 10.1097/01.CCM.0000260626.23848.FC.
  42. Chardoli M, Heidari F, Rabiee H, Sharif-Alhoseini M, Shokoohi H, Rahimi-Movaghar V. Echocardiography integrated ACLS protocol ver- sus conventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest. Chin J Traumatol. 2012;15:284–287.
  43. Ornato JP, Garnett AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med. 1990; 19:1104–1106.
  44. Chandra NC, Gruben KG, Tsitlik JE, Brower R, Guerci AD, Halperin HH, Weisfeldt ML, Permutt S. Observations of ventilation during resuscitation in a canine model. Circulation. 1994;90:3070–3075.
  45. Bailey AR, Hett DA. The laryngeal mask airway in resuscitation. Resuscitation. 1994;28:107–110.
  46. Dorges V, Wenzel V, Knacke P, Gerlach K. Comparison of different airway management strategies to ventilate apneic, nonpreoxygenated patients. Crit Care Med. 2003;31:800–804.
  47. Doerges V, Sauer C, Ocker H, Wenzel V, Schmucker P. Airway management during cardiopulmonary resuscitation—a comparative study of bag-valve-mask, laryngeal mask airway and combitube in a bench model. Resuscitation. 1999;41:63–69.
  48. Weiler N, Heinrichs W, Dick W. Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation. Prehosp Disaster Med. 1995;10:101–105.
  49. Ocker H, Wenzel V, Schmucker P, Dorges V. Effectiveness of various airway management techniques in a bench model simulating a cardiac arrest patient. J Emerg Med. 2001;20:7–12.
  50. Hasegawa K, Hiraide A, Chang Y, Brown DF. Association of prehospital advanced airway management with neurologic outcome and survival in patients with out-of-hospital cardiac arrest. JAMA. 2013;309:257–266. doi: 10.1001/jama.2012.187612.
  51. Holmberg M, Holmberg S, Herlitz J. Low chance of survival among patients requiring adrenaline (epinephrine) or intubation after out-of-hos- pital cardiac arrest in Sweden. Resuscitation. 2002;54:37–45.
  52. McMullan J, Gerecht R, Bonomo J, Robb R, McNally B, Donnelly J, Wang HE; CARES Surveillance Group. Airway management and out- of-hospital cardiac arrest outcome in the CARES registry. Resuscitation. 2014;85:617–622. doi: 10.1016/j.resuscitation.2014.02.007.
  53. Shin SD, Ahn KO, Song KJ, Park CB, Lee EJ. Out-of-hospital air- way management and cardiac arrest outcomes: a propensity score matched analysis. Resuscitation. 2012;83:313–319. doi: 10.1016/j. resuscitation.2011.10.028.
  54. Hanif MA, Kaji AH, Niemann JT. Advanced airway management does not improve outcome of out-of-hospital cardiac arrest. Acad Emerg Med. 2010;17:926–931. doi: 10.1111/j.1553-2712.2010.00829.x.
  55. Adams JN, Sirel J, Marsden K, Cobbe SM. Heartstart Scotland: the use of paramedic skills in out of hospital resuscitation. Heart. 1997;78:399–402.
  56. Studnek JR, Thestrup L, Vandeventer S, Ward SR, Staley K, Garvey L, Blackwell T. The association between prehospital endotracheal intuba- tion attempts and survival to hospital discharge among out-of-hospi- tal cardiac arrest patients. Acad Emerg Med. 2010;17:918–925. doi: 10.1111/j.1553-2712.2010.00827.x.
  57. Takei Y, Enami M, Yachida T, Ohta K, Inaba H. Tracheal intubation by paramedics under limited indication criteria may improve the short-term outcome of out-of-hospital cardiac arrests with noncardiac origin. J Anesth. 2010;24:716–725. doi: 10.1007/s00540-010-0974-6.
  58. Yeung J, Chilwan M, Field R, Davies R, Gao F, Perkins GD. The impact of airway management on quality of cardiopulmonary resuscitation: an observational study in patients during cardiac arrest. Resuscitation. 2014;85:898–904. doi: 10.1016/j.resuscitation.2014.02.018.
  59. Petito SP, Russell WJ. The prevention of gastric inflation—a neglected benefit of cricoid pressure. Anaesth Intensive Care. 1988;16:139–143.
  60. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric insufflation and rapid sequence induction. Br J Anaesth. 1987;59:315–318.
  61. Salem MR, Wong AY, Mani M, Sellick BA. Efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in pediatric patients. Anesthesiology. 1974;40:96–98.
  62. Moynihan RJ, Brock-Utne JG, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insufflation in infants and children. Anesthesiology. 1993;78:652–656.
  63. Asai T, Goy RW, Liu EH. Cricoid pressure prevents placement of the laryngeal tube and laryngeal tube-suction II. Br J Anaesth. 2007;99:282–285.
  64. Turgeon AF, Nicole PC, Trepanier CA, Marcoux S, Lessard MR. Cricoid pressure does not increase the rate of failed intubation by direct laryngoscopy in adults. Anesthesiology. 2005;102:315–319.
  65. Allman KG. The effect of cricoid pressure application on airway patency. J Clin Anesth. 1995;7:197–199.
  66. Brimacombe J, White A, Berry A. Effect of cricoid pressure on ease of insertion of the laryngeal mask airway. Br J Anaesth. 1993;71:800–802.
  67. McNelis U, Syndercombe A, Harper I, Duggan J. The effect of cricoid pressure on intubation facilitated by the gum elastic bougie. Anaesthesia. 2007;62:456–459.
  68. Hartsilver EL, Vanner RG. Airway obstruction with cricoid pressure. Anaesthesia. 2000;55:208–211.
  69. Hocking G, Roberts FL, Thew ME. Airway obstruction with cricoid pressure and lateral tilt. Anaesthesia. 2001;56:825–828.
  70. Stoneham MD. The nasopharyngeal airway. Assessment of position by fibreoptic laryngoscopy. Anaesthesia. 1993;48:575–580.
  71. Schade K, Borzotta A, Michaels A. Intracranial malposition of nasopharyngeal airway. J Trauma. 2000;49:967–968.
  72. Muzzi DA, Losasso TJ, Cucchiara RF. Complication from a nasopharyngeal airway in a patient with a basilar skull fracture. Anesthesiology. 1991;74:366–368.
  73. Wong ML, Carey S, Mader TJ, Wang HE. Time to invasive airway placement and resuscitation outcomes after inhospital cardiopulmonary arrest. Resuscitation. 2010;81:182–186.
  74. Shy BD, Rea TD, Becker LJ, Eisenberg MS. Time to intubation and survival in prehospital cardiac arrest. Prehosp Emerg Care. 2004;8:394–399.
  75. Jennings PA, Cameron P, Walker T, Bernard S, Smith K. Out-of-hospital cardiac arrest in Victoria: rural and urban outcomes. Med J Aust. 2006;185:135–139.
  76. Dumot JA, Burval DJ, Sprung J, Waters JH, Mraovic B, Karafa MT, Mascha EJ, Bourke DL. Outcome of adult cardiopulmonary resuscitations at a tertiary referral center including results of “limited” resuscitations. Arch Intern Med. 2001;161:1751–1758.
  77. Bobrow BJ, Ewy GA, Clark L, Chikani V, Berg RA, Sanders AB, Vadeboncoeur TF, Hilwig RW, Kern KB. Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest. Ann Emerg Med. 2009;54:656–662.
  78. Goldenberg IF, Campion BC, Siebold CM, McBride JW, Long LA. Esophageal gastric tube airway vs endotracheal tube in prehospital cardio- pulmonary arrest. Chest. 1986;90:90–96.
  79. Rabitsch W, Schellongowski P, Staudinger T, Hofbauer R, Dufek V, Eder B, Raab H, Thell R, Schuster E, Frass M. Comparison of a conventional tracheal airway with the Combitube in an urban emergency medical ser- vices system run by physicians. Resuscitation. 2003;57:27–32.
  80. Cady CE, Weaver MD, Pirrallo RG, Wang HE. Effect of emergency medical technician-placed Combitubes on outcomes after out-of-hospital cardiopulmonary arrest. Prehosp Emerg Care. 2009;13:495–499. doi: 10.1080/10903120903144874.
  81. Kajino K, Iwami T, Kitamura T, Daya M, Ong ME, Nishiuchi T, Hayashi Y, Sakai T, Shimazu T, Hiraide A, Kishi M, Yamayoshi S. Comparison of supraglottic airway versus endotracheal intubation for the pre-hospital treatment of out-of-hospital cardiac arrest. Crit Care. 2011;15:R236. doi: 10.1186/cc10483.
  82. Wang HE, Szydlo D, Stouffer JA, Lin S, Carlson JN, Vaillancourt C, Sears G, Verbeek RP, Fowler R, Idris AH, Koenig K, Christenson J, Minokadeh A, Brandt J, Rea T; ROC Investigators. Endotracheal intubation versus supra- glottic airway insertion in out-of-hospital cardiac arrest. Resuscitation. 2012;83:1061–1066. doi: 10.1016/j.resuscitation.2012.05.018.
  83. Tanabe S, Ogawa T, Akahane M, Koike S, Horiguchi H, Yasunaga H, Mizoguchi T, Hatanaka T, Yokota H, Imamura T. Comparison of neu- rological outcome between tracheal intubation and supraglottic airway device insertion of out-of-hospital cardiac arrest patients: a nationwide, population-based, observational study. J Emerg Med. 2013;44:389–397. doi: 10.1016/j.jemermed.2012.02.026.
  84. Warner KJ, Carlbom D, Cooke CR, Bulger EM, Copass MK, Sharar SR. Paramedic training for proficient prehospital endotracheal intubation. Prehosp Emerg Care. 2010;14:103–108.
  85. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med. 2002;28:701– 704. doi: 10.1007/s00134-002-1290-x.
  86. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, Tanaka K. The assessment of three methods to verify tracheal tube placement in the emer- gency setting. Resuscitation. 2003;56:153–157.
  87. Tanigawa K, Takeda T, Goto E, Tanaka K. Accuracy and reliability of the self-inflating bulb to verify tracheal intubation in out-of-hospital cardiac arrest patients. Anesthesiology. 2000;93:1432–1436.
  88. Ward KR, Yealy DM. End-tidal carbon dioxide monitoring in emergency medicine, Part 2: Clinical applications. Acad Emerg Med. 1998;5:637–646.
  89. Tobias JD, Meyer DJ. Noninvasive monitoring of carbon dioxide during respiratory failure in toddlers and infants: end-tidal versus transcutaneous carbon dioxide. Anesth Analg. 1997;85:55–58.
  90. Bozeman WP, Hexter D, Liang HK, Kelen GD. Esophageal detector device versus detection of end-tidal carbon dioxide level in emergency intubation. Ann Emerg Med. 1996;27:595–599.
  91. Hayden SR, Sciammarella J, Viccellio P, Thode H, Delagi R. Colorimetric end-tidal CO2 detector for verification of endotracheal tube placement in out-of-hospital cardiac arrest. Acad Emerg Med. 1995;2:499–502.
  92. MacLeod BA, Heller MB, Gerard J, Yealy DM, Menegazzi JJ. Verification of endotracheal tube placement with colorimetric end-tidal CO2 detection. Ann Emerg Med. 1991;20:267–270.
  93. Anton WR, Gordon RW, Jordan TM, Posner KL, Cheney FW. A disposable end-tidal CO2 detector to verify endotracheal intubation. Ann Emerg Med. 1991;20:271–275.
  94. Sanders KC, Clum WB 3rd, Nguyen SS, Balasubramaniam S. End-tidal carbon dioxide detection in emergency intubation in four groups of patients. J Emerg Med. 1994;12:771–777.
  95. Tanigawa K, Takeda T, Goto E, Tanaka K. The efficacy of esophageal detector devices in verifying tracheal tube placement: a randomized cross-over study of out-of-hospital cardiac arrest patients. Anesth Analg. 2001;92:375–378.
  96. Oberly D, Stein S, Hess D, Eitel D, Simmons M. An evaluation of the esophageal detector device using a cadaver model. Am J Emerg Med. 1992;10:317–320.
  97. Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experience with the syringe esophageal detector device. Acad Emerg Med. 1997;4:563–568.
  98. Chou HC, Tseng WP, Wang CH, Ma MH, Wang HP, Huang PC, Sim SS, Liao YC, Chen SY, Hsu CY, Yen ZS, Chang WT, Huang CH, Lien WC, Chen SC. Tracheal rapid ultrasound exam (T.R.U.E.) for confirming endotracheal tube placement during emergency intubation. Resuscitation. 2011;82:1279–1284. doi: 10.1016/j.resuscitation.2011.05.016.
  99. Zadel S, Strnad M, Prosen G, Mekiš D. Point of care ultrasound for orotra- cheal tube placement assessment in out-of hospital setting. Resuscitation. 2015;87:1–6. doi: 10.1016/j.resuscitation.2014.11.006.
  100. Chou HC, Chong KM, Sim SS, Ma MH, Liu SH, Chen NC, Wu MC, Fu CM, Wang CH, Lee CC, Lien WC, Chen SC. Real-time tracheal ultrasonography for confirmation of endotracheal tube placement during cardiopulmonary resuscitation. Resuscitation. 2013;84:1708–1712. doi: 10.1016/j.resuscitation.2013.06.018.
  101. Yap SJ, Morris RW, Pybus DA. Alterations in endotracheal tube position during general anaesthesia. Anaesth Intensive Care. 1994;22:586–588.
  102. Sugiyama K, Yokoyama K. Displacement of the endotracheal tube caused by change of head position in pediatric anesthesia: evaluation by fiberoptic bronchoscopy. Anesth Analg. 1996;82:251–253.
  103. King HK. A new device: Tube Securer. An endotracheal tube holder with integrated bite-block. Acta Anaesthesiol Sin. 1997;35:257–259.
  104. Falk JL, Sayre MR. Confirmation of airway placement. Prehosp Emerg Care. 1999;3:273–278.
  105. Wang HE, Kupas DF, Paris PM, Bates RR, Yealy DM. Preliminary experience with a prospective, multi-centered evaluation of out-of-hospital endotracheal intubation. Resuscitation. 2003;58:49–58.
  106. Kupas DF, Kauffman KF, Wang HE. Effect of airway-securing method on prehospital endotracheal tube dislodgment. Prehosp Emerg Care. 2010;14:26–30.
  107. Levy H, Griego L. A comparative study of oral endotracheal tube securing methods. Chest. 1993;104:1537–1540.
  108. Tasota FJ, Hoffman LA, Zullo TG, Jamison G. Evaluation of two methods used to stabilize oral endotracheal tubes. Heart Lung. 1987;16:140–146.
  109. Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, Sparks CW, Conrad CJ, Provo TA, Lurie KG. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation. 2004;109:1960–1965. doi: 10.1161/01. CIR.0000126594.79136.61.
  110. O’Neill JF, Deakin CD. Do we hyperventilate cardiac arrest patients? Resuscitation. 2007;73:82–85. doi: 10.1016/j.resuscitation.2006.09.012.
  111. Sanders AB, Kern KB, Berg RA, Hilwig RW, Heidenrich J, Ewy GA. Survival and neurologic outcome after cardiopulmonary resuscitation with four differ- ent chest compression-ventilation ratios. Ann Emerg Med. 2002;40:553–562.
  112. Aufderheide TP, Lurie KG. Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med. 2004;32(9 suppl):S345–S351.
  113. Yannopoulos D, Sigurdsson G, McKnite S, Benditt D, Lurie KG. Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest. Resuscitation. 2004;61:75–82. doi: 10.1016/j.resuscitation.2003.12.006.
  114. Yannopoulos D, Aufderheide TP, Gabrielli A, Beiser DG, McKnite SH, Pirrallo RG, Wigginton J, Becker L, Vanden Hoek T, Tang W, Nadkarni VM, Klein JP, Idris AH, Lurie KG. Clinical and hemodynamic compari- son of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmo- nary resuscitation. Crit Care Med. 2006;34:1444–1449. doi: 10.1097/01. CCM.0000216705.83305.99.
  115. Hayes MM, Ewy GA, Anavy ND, Hilwig RW, Sanders AB, Berg RA, Otto CW, Kern KB. Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out- of-hospital ventricular fibrillation. Resuscitation. 2007;74:357–365. doi: 10.1016/j.resuscitation.2007.01.004.
  116. Cavus E, Meybohm P, Bein B, Steinfath M, Pöppel A, Wenzel V, Scholz J, Dörges V. Impact of different compression-ventilation ratios during basic life support cardiopulmonary resuscitation. Resuscitation. 2008;79:118– 124. doi: 10.1016/j.resuscitation.2008.04.015.
  117. Hwang SO, Kim SH, Kim H, Jang YS, Zhao PG, Lee KH, Choi HJ, Shin TY. Comparison of 15:1, 15:2, and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation in a canine model of a simu- lated, witnessed cardiac arrest. Acad Emerg Med. 2008;15:183–189. doi: 10.1111/j.1553-2712.2008.00026.x.
  118. Gazmuri RJ, Ayoub IM, Radhakrishnan J, Motl J, Upadhyaya MP. Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO2. Resuscitation. 2012;83:259–264. doi: 10.1016/j.resuscitation.2011.07.034.
  119. Kill C, Hahn O, Dietz F, Neuhaus C, Schwarz S, Mahling R, Wallot P, Jerrentrup A, Steinfeldt T, Wulf H, Dersch W. Mechanical ventilation during cardiopulmonary resuscitation with intermittent positive-pressure ventilation, bilevel ventilation, or chest compression synchronized ven- tilation in a pig model. Crit Care Med. 2014;42:e89–e95. doi: 10.1097/ CCM.0b013e3182a63fa0.
  120. Abella BS, Alvarado JP, Myklebust H, Edelson DP, Barry A, O’Hearn N, Vanden Hoek TL, Becker LB. Quality of cardiopulmonary resusci- tation during in-hospital cardiac arrest. JAMA. 2005;293:305–310. doi: 10.1001/jama.293.3.305.
  121. Weiss SJ, Ernst AA, Jones R, Ong M, Filbrun T, Augustin C, Barnum M, Nick TG. Automatic transport ventilator versus bag valve in the EMS setting: a prospective, randomized trial. South Med J. 2005;98:970–976.
  122. Johannigman JA, Branson RD, Johnson DJ, Davis K Jr., Hurst JM. Out-of-hospital ventilation: bag-valve device vs transport ventilator. Acad Emerg Med. 1995;2:719–724.
  123. Rea TD, Cook AJ, Stiell IG, Powell J, Bigham B, Callaway CW, Chugh S, Aufderheide TP, Morrison L, Terndrup TE, Beaudoin T, Wittwer L, Davis D, Idris A, Nichol G. Predicting survival after out-of-hospital cardiac arrest: role of the Utstein data elements. Ann Emerg Med. 2010;55:249–257.
  124. Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2010;3:63–81.
  125. Agarwal DA, Hess EP, Atkinson EJ, White RD. Ventricular fibrillation in Rochester, Minnesota: experience over 18 years. Resuscitation. 2009;80:1253–1258.
  126. Chan PS, Nichol G, Krumholz HM, Spertus JA, Nallamothu BK. Hospital variation in time to defibrillation after in-hospital cardiac arrest. Arch Intern Med. 2009;169:1265–1273.
  127. Caffrey SL, Willoughby PJ, Pepe PE, Becker LB. Public use of automated external defibrillators. N Engl J Med. 2002;347:1242–1247.
  128. Valenzuela TD, Roe DJ, Nichol G, Clark LL, Spaite DW, Hardman RG. Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos. N Engl J Med. 2000;343:1206–1209.
  129. Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, Hallstrom AP, Murray WA, Olsufka M, Walsh T. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341:871–878.
  130. Vandycke C, Martens P. High dose versus standard dose epinephrine in cardiac arrest—a meta-analysis. Resuscitation. 2000;45:161–166.
  131. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884–890.
  132. Stiell IG, Wells GA, Field B, Spaite DW, Nesbitt LP, De Maio VJ, Nichol G, Cousineau D, Blackburn J, Munkley D, Luinstra-Toohey L, Campeau T, Dagnone E, Lyver M. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med. 2004;351:647–656.
  133. Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L. Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA. 2009;302:2222–2229.
  134. Morrison LJ, Henry RM, Ku V, Nolan JP, Morley P, Deakin CD. Single-shock defibrillation success in adult cardiac arrest: a sys- tematic review. Resuscitation. 2013;84:1480–1486. doi: 10.1016/j. resuscitation.2013.07.008.
  135. Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J fixed-energy defibrillation protocol treats recurrent ventricular fibrilla- tion (VF) as effectively as initial VF. Resuscitation. 2008;79:28–33. doi: 10.1016/j.resuscitation.2008.04.028.
  136. Koster RW, Walker RG, Chapman FW. Recurrent ventricular fibril- lation during advanced life support care of patients with prehospi- tal cardiac arrest. Resuscitation. 2008;78:252–257. doi: 10.1016/j. resuscitation.2008.03.231.
  137. Hess EP, Agarwal D, Myers LA, Atkinson EJ, White RD. Performance of a rectilinear biphasic waveform in defibrillation of presenting and recurrent ventricular fibrillation: a prospective multicenter study. Resuscitation. 2011;82:685–689. doi: 10.1016/j.resuscitation.2011.02.008.
  138. Jost D, Degrange H, Verret C, Hersan O, Banville IL, Chapman FW, Lank P, Petit JL, Fuilla C, Migliani R, Carpentier JP; DEFI 2005 Work Group. DEFI 2005: a randomized controlled trial of the effect of automated external defibrillator cardiopulmonary resuscitation pro- tocol on outcome from out-of-hospital cardiac arrest. Circulation. 2010;121:1614–1622. doi: 10.1161/CIRCULATIONAHA.109.878389.
  139. Berdowski J, ten Haaf M, Tijssen JG, Chapman FW, Koster RW. Time in recurrent ventricular fibrillation and survival after out-of-hospi- tal cardiac arrest. Circulation. 2010;122:1101–1108. doi: 10.1161/ CIRCULATIONAHA.110.958173.
  140. Berdowski J, Tijssen JG, Koster RW. Chest compressions cause recurrence of ventricular fibrillation after the first successful conver- sion by defibrillation in out-of-hospital cardiac arrest. Circ Arrhythm Electrophysiol. 2010;3:72–78. doi: 10.1161/CIRCEP.109.902114.
  141. Conover Z, Kern KB, Silver AE, Bobrow BJ, Spaite DW, Indik JH. Resumption of chest compressions after successful defibrillation and risk for recurrence of ventricular fibrillation in out-of-hospital cardiac arrest. Circ Arrhythm Electrophysiol. 2014;7:633–639. doi: 10.1161/ CIRCEP.114.001506.
  142. Hoogendijk MG, Schumacher CA, Belterman CN, Boukens BJ, Berdowski J, de Bakker JM, Koster RW, Coronel R. Ventricular fibril- lation hampers the restoration of creatine-phosphate levels during simu- lated cardiopulmonary resuscitations. Europace. 2012;14:1518–1523. doi: 10.1093/europace/eus078.
  143. Pytte M, Pedersen TE, Ottem J, Rokvam AS, Sunde K. Comparison of hands-off time during CPR with manual and semi-automatic defibrillation in a manikin model. Resuscitation. 2007;73:131–136.
  144. Kramer-Johansen J, Edelson DP, Abella BS, Becker LB, Wik L, Steen PA. Pauses in chest compression and inappropriate shocks: a comparison of manual and semi-automatic defibrillation attempts. Resuscitation. 2007;73:212–220.
  145. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest. Circulation. 2004;110:10–15.
  146. Box MS, Watson JN, Addison PS, Clegg GR, Robertson CE. Shock outcome prediction before and after CPR: a comparative study of manual and automated active compression-decompression CPR. Resuscitation. 2008;78:265–274.
  147. Brown CG, Dzwonczyk R, Martin DR. Physiologic measurement of the ventricular fibrillation ECG signal: estimating the duration of ventricular fibrillation. Ann Emerg Med. 1993;22:70–74.
  148. Callaway CW, Sherman LD, Mosesso VN Jr., Dietrich TJ, Holt E, Clarkson MC. Scaling exponent predicts defibrillation success for out-of-hospital ventricular fibrillation cardiac arrest. Circulation. 2001;103:1656–1661.
  149. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. Predicting outcome of defibrillation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest. Circulation. 2000;102:1523–1529.
  150. Eftestol T, Losert H, Kramer-Johansen J, Wik L, Sterz F, Steen PA. Independent evaluation of a defibrillation outcome predictor for out-of-hospital cardiac arrested patients. Resuscitation. 2005;67:55–61.
  151. Gundersen K, Kvaloy JT, Kramer-Johansen J, Olasveengen TM, Eilevstjonn J, Eftestol T. Using within-patient correlation to improve the accuracy of shock outcome prediction for cardiac arrest. Resuscitation. 2008;78:46–51.
  152. Gunderson EP. Breast-feeding and diabetes: long-term impact on mothers and their infants. Curr Diab Rep. 2008;8:279–286.
  153. Gundersen K, Kvaloy JT, Kramer-Johansen J, Steen PA, Eftestol T. Development of the probability of return of spontaneous circulation in intervals without chest compressions during out-of-hospital cardiac arrest: an observational study. BMC Med. 2009;7:6.
  154. Jekova I, Mougeolle F, Valance A. Defibrillation shock success estimation by a set of six parameters derived from the electrocardiogram. Physiol Meas. 2004;25:1179–1188.
  155. Neurauter A, Eftestol T, Kramer-Johansen J, Abella BS, Sunde K, Wenzel V, Lindner KH, Eilevstjonn J, Myklebust H, Steen PA, Strohmenger HU. Prediction of countershock success using single features from multiple ventricular fibrillation frequency bands and feature combinations using neural networks. Resuscitation. 2007;73:253–263.
  156. Olasveengen TM, Eftestol T, Gundersen K, Wik L, Sunde K. Acute ischemic heart disease alters ventricular fibrillation waveform characteristics in out-of hospital cardiac arrest. Resuscitation. 2009;80:412–417.
  157. Ristagno G, Gullo A, Berlot G, Lucangelo U, Geheb E, Bisera J. Prediction of successful defibrillation in human victims of out-of-hospital cardiac arrest: a retrospective electrocardiographic analysis. Anaesth Intensive Care. 2008;36:46–50.
  158. Russell ME, Friedman MI, Mascioli SR, Stolz LE. Off-label use: an industry perspective on expanding use beyond approved indications. J Interv Cardiol. 2006;19:432–438.
  159. Snyder DE, White RD, Jorgenson DB. Outcome prediction for guidance of initial resuscitation protocol: shock first or CPR first. Resuscitation. 2007;72:45–51.
  160. Watson JN, Uchaipichat N, Addison PS, Clegg GR, Robertson CE, Eftestol T, Steen PA. Improved prediction of defibrillation success for out-of-hospital VF cardiac arrest using wavelet transform methods. Resuscitation. 2004;63:269–275.
  161. Watson JN, Addison PS, Clegg GR, Steen PA, Robertson CE. Practical issues in the evaluation of methods for the prediction of shock outcome success in out-of-hospital cardiac arrest patients. Resuscitation. 2006;68:51–59.
  162. Weaver WD, Cobb LA, Dennis D, Ray R, Hallstrom AP, Copass MK. Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest. Ann Intern Med. 1985;102:53–55.
  163. Yang Z, Lu W, Harrison RG, Eftestol T, Steen PA. A probabilistic neural network as the predictive classifier of out-of-hospital defibrillation outcomes. Resuscitation. 2005;64:31–36.
  164. Jagric T, Marhl M, Stajer D, Kocjancic ST, Podbregar M, Perc M. Irregularity test for very short electrocardiogram (ECG) signals as a method for predicting a successful defibrillation in patients with ventricular fibrillation. Transl Res. 2007;149:145–151.
  165. Strohmenger HU, Lindner KH, Brown CG. Analysis of the ventricular fibrillation ECG signal amplitude and frequency parameters as predictors of countershock success in humans. Chest. 1997;111:584–589.
  166. Porter TR, Ornato JP, Guard CS, Roy VG, Burns CA, Nixon JV. Transesophageal echocardiography to assess mitral valve function and flow during cardiopulmonary resuscitation. Am J Cardiol. 1992;70:1056–1060.
  167. Agostoni P, Cornelis K, Vermeersch P. Successful percutaneous treatment of an intraprocedural left main stent thrombosis with the support of an automatic mechanical chest compression device. Int J Cardiol. 2008;124:e19–e21.
  168. Grogaard HK, Wik L, Eriksen M, Brekke M, Sunde K. Continuous mechanical chest compressions during cardiac arrest to facilitate restoration of coronary circulation with percutaneous coronary intervention. J Am Coll Cardiol. 2007;50:1093–1094.
  169. Steen S, Sjoberg T, Olsson P, Young M. Treatment of out-of-hospital cardiac arrest with LUCAS, a new device for automatic mechanical compression and active decompression resuscitation. Resuscitation. 2005;67:25–30.
  170. Larsen AI, Hjornevik AS, Ellingsen CL, Nilsen DW. Cardiac arrest with continuous mechanical chest compression during percutaneous coronary intervention. A report on the use of the LUCAS device. Resuscitation. 2007;75:454–459.
  171. Wagner H, Terkelsen CJ, Friberg H, Harnek J, Kern K, Lassen JF, Olivecrona GK. Cardiac arrest in the catheterisation laboratory: a 5-year experience of using mechanical chest compressions to facilitate PCI during prolonged resuscitation efforts. Resuscitation. 2010;81:383–387.
  172. Criley JM, Blaufuss AH, Kissel GL. Cough-induced cardiac compression: self-administered form of cardiopulmonary resuscitation. JAMA. 1976;236:1246–1250.
  173. Criley JM, Blaufuss AH, Kissel GL. Self-administered cardiopulmonary resuscitation by cough-induced cardiac compression. Trans Am Clin Climatol Assoc. 1976;87:138–146.
  174. Miller B, Lesnefsky E, Heyborne T, Schmidt B, Freeman K, Breckinridge S, Kelley K, Mann D, Reiter M. Cough-cardiopulmonary resuscitation in the cardiac catheterization laboratory: hemodynamics during an episode of prolonged hypotensive ventricular tachycardia. Cathet Cardiovasc Diagn. 1989;18:168–171.
  175. Keeble W, Tymchak WJ. Triggering of the Bezold Jarisch Reflex by reperfusion during primary PCI with maintenance of consciousness by cough CPR: a case report and review of pathophysiology. J Invasive Cardiol. 2008;20:E239–E242.
  176. Saba SE, David SW. Sustained consciousness during ventricular fibrillation: case report of cough cardiopulmonary resuscitation. Cathet Cardiovasc Diagn. 1996;37:47–48.
  177. Bottiger BW, Arntz HR, Chamberlain DA, Bluhmki E, Belmans A, Danays T, Carli PA, Adgey JA, Bode C, Wenzel V. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359:2651–2662.
  178. Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, Hallstrom AP, Murray WA, Olsufka M, Walsh T. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341:871–878. doi: 10.1056/ NEJM199909163411203.
  179. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ven- tricular fibrillation. N Engl J Med. 2002;346:884–890. doi: 10.1056/ NEJMoa013029.
  180. Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, Lindkvist J, Persson NG, Holmberg S. Lidocaine in out-of-hospital ventricular fibril- lation. Does it improve survival? Resuscitation. 1997;33:199–205.
  181. Harrison EE. Lidocaine in prehospital countershock refractory ventricu- lar fibrillation. Ann Emerg Med. 1981;10:420–423.
  182. Markel DT, Gold LS, Allen J, Fahrenbruch CE, Rea TD, Eisenberg MS, Kudenchuk PJ. Procainamide and survival in ventricular fibrillation out-of-hospital cardiac arrest. Acad Emerg Med. 2010;17:617–623. doi: 10.1111/j.1553-2712.2010.00763.x.
  183. Fatovich DM, Prentice DA, Dobb GJ. Magnesium in cardiac arrest (the magic trial). Resuscitation. 1997;35:237–241.
  184. Allegra J, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, Yablonski M. Magnesium sulfate in the treat- ment of refractory ventricular fibrillation in the prehospital setting. Resuscitation. 2001;49:245–249.
  185. Hassan TB, Jagger C, Barnett DB. A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation. Emerg Med J. 2002;19:57–62.
  186. Thel MC, Armstrong AL, McNulty SE, Califf RM, O’Connor CM. Randomised trial of magnesium in in-hospital cardiac arrest. Duke Internal Medicine Housestaff. Lancet. 1997;350:1272–1276.
  187. Skrifvars MB, Pettilä V, Rosenberg PH, Castrén M. A multiple logistic regression analysis of in-hospital factors related to survival at six months in patients resuscitated from out-of-hospital ventricular fibrillation. Resuscitation. 2003;59:319–328.
  188. Sadowski ZP, Alexander JH, Skrabucha B, Dyduszynski A, Kuch J, Nartowicz E, Swiatecka G, Kong DF, Granger CB. Multicenter random- ized trial and a systematic overview of lidocaine in acute myocardial infarction. Am Heart J. 1999;137:792–798.
  189. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials. JAMA. 1993;270:1589–1595.
  190. Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation. 2013;84:1512–1518. doi: 10.1016/j.resuscitation.2013.05.022.
  191. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82:1138– 1143. doi: 10.1016/j.resuscitation.2011.06.029.
  192. Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of- hospital cardiac arrest. JAMA. 2012;307:1161–1168. doi: 10.1001/ jama.2012.294.
  193. Machida M, Miura S, Matsuo K, Ishikura H, Saku K. Effect of intrave- nous adrenaline before arrival at the hospital in out-of-hospital cardiac arrest. J Cardiol. 2012;60:503–507. doi: 10.1016/j.jjcc.2012.07.001.
  194. Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J. A randomized clinical trial of high-dose epinephrine and norepineph- rine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA. 1992;268:2667–2672.
  195. Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, Carli P. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest out- side the hospital. European Epinephrine Study Group. N Engl J Med. 1998;339:1595–1601. doi: 10.1056/NEJM199811263392204.
  196. Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, Jastremski M. A comparison of standard-dose and high-dose epineph- rine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group. N Engl J Med. 1992;327:1051–1055. doi: 10.1056/NEJM199210083271503.
  197. Sherman BW, Munger MA, Foulke GE, Rutherford WF, Panacek EA. High-dose versus standard-dose epinephrine treatment of car- diac arrest after failure of standard therapy. Pharmacotherapy. 1997;17:242–247.
  198. Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, Dickinson GE. High-dose epinephrine in adult cardiac arrest. N Engl J Med. 1992;327:1045–1050. doi: 10.1056/ NEJM199210083271502.
  199. Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, Petit P. Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital. Resuscitation. 1995;29:3–9.
  200. Maturi MF, Martin SE, Markle D, Maxwell M, Burruss CR, Speir E, Greene R, Ro YM, Vitale D, Green MV. Coronary vasoconstric- tion induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels. Circulation. 1991;83:2111–2121.
  201. Asfar P, Radermacher P. Vasopressin and ischaemic heart disease: more than coronary vasoconstriction? Crit Care. 2009;13:169. doi: 10.1186/cc7954.
  202. Feng JJ, Arendshorst WJ. Enhanced renal vasoconstriction induced by vasopressin in SHR is mediated by V1 receptors. Am J Physiol. 1996;271(2 pt 2):F304–F313.
  203. Mukoyama T, Kinoshita K, Nagao K, Tanjoh K. Reduced effective- ness of vasopressin in repeated doses for patients undergoing prolonged cardiopulmonary resuscitation. Resuscitation. 2009;80:755–761. doi: 10.1016/j.resuscitation.2009.04.005.
  204. Gueugniaud PY, David JS, Chanzy E, Hubert H, Dubien PY, Mauriaucourt P, Bragança C, Billères X, Clotteau-Lambert MP, Fuster P, Thiercelin D, Debaty G, Ricard-Hibon A, Roux P, Espesson C, Querellou E, Ducros L, Ecollan P, Halbout L, Savary D, Guillaumée F, Maupoint R, Capelle P, Bracq C, Dreyfus P, Nouguier P, Gache A, Meurisse C, Boulanger B, Lae C, Metzger J, Raphael V, Beruben A, Wenzel V, Guinhouya C, Vilhelm C, Marret E. Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation. N Engl J Med. 2008;359:21–30. doi: 10.1056/NEJMoa0706873.
  205. Ong ME, Tiah L, Leong BS, Tan EC, Ong VY, Tan EA, Poh BY, Pek PP, Chen Y. A randomised, double-blind, multi-centre trial comparing vasopressin and adrenaline in patients with cardiac arrest presenting to or in the Emergency Department. Resuscitation. 2012;83:953–960. doi: 10.1016/j.resuscitation.2012.02.005.
  206. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH; European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study Group. A comparison of vasopressin and epineph- rine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004;350:105–113. doi: 10.1056/NEJMoa025431.
  207. Ducros L, Vicaut E, Soleil C, Le Guen M, Gueye P, Poussant T, Mebazaa A, Payen D, Plaisance P. Effect of the addition of vasopressin or vasopressin plus nitroglycerin to epinephrine on arterial blood pres- sure during cardiopulmonary resuscitation in humans. J Emerg Med. 2011;41:453–459. doi: 10.1016/j.jemermed.2010.02.030.
  208. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, Lindner IM, Lurie KG. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet. 1997;349:535–537. doi: 10.1016/S0140-6736(97)80087-6.
  209. Callaway CW, Hostler D, Doshi AA, Pinchalk M, Roth RN, Lubin J, Newman DH, Kelly LJ. Usefulness of vasopressin administered with epinephrine during out-of-hospital cardiac arrest. Am J Cardiol. 2006;98:1316–1321. doi: 10.1016/j.amjcard.2006.06.022.
  210. Donnino MW, Salciccioli JD, Howell MD, Cocchi MN, Giberson B, Berg K, Gautam S, Callaway C; American Heart Association’s Get With The Guidelines-Resuscitation Investigators. Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shock- able rhythms: retrospective analysis of large in-hospital data registry. BMJ. 2014;348:g3028.
  211. Goto Y, Maeda T, Goto Y. Effects of prehospital epinephrine during out- of-hospital cardiac arrest with initial non-shockable rhythm: an observa- tional cohort study. Crit Care. 2013;17:R188. doi: 10.1186/cc12872.
  212. Nakahara S, Tomio J, Nishida M, Morimura N, Ichikawa M, Sakamoto T. Association between timing of epinephrine administration and intact neurologic survival following out-of-hospital cardiac arrest in Japan: a population-based prospective observational study. Acad Emerg Med. 2012;19:782–792. doi: 10.1111/j.1553-2712.2012.01387.x.
  213. Koscik C, Pinawin A, McGovern H, Allen D, Media DE, Ferguson T, Hopkins W, Sawyer KN, Boura J, Swor R. Rapid epineph- rine administration improves early outcomes in out-of-hospital cardiac arrest. Resuscitation. 2013;84:915–920. doi: 10.1016/j. resuscitation.2013.03.023.
  214. Hayashi Y, Iwami T, Kitamura T, Nishiuchi T, Kajino K, Sakai T, Nishiyama C, Nitta M, Hiraide A, Kai T. Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest. Circ J. 2012;76:1639–1645.
  215. Cantrell CL Jr, Hubble MW, Richards ME. Impact of delayed and infrequent administration of vasopressors on return of spontaneous circulation during out-of-hospital cardiac arrest. Prehosp Emerg Care. 2013;17:15–22. doi: 10.3109/10903127.2012.702193.
  216. Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, Katsios N, Papastylianou A, Gkisioti S, Stathopoulos A, Kollintza A, Stamataki E, Roussos C. Vasopressin, epinephrine, and corticosteroids for in- hospital cardiac arrest. Arch Intern Med. 2009;169:15–24. doi: 10.1001/ archinternmed.2008.509.
  217. Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG. Vasopressin, steroids, and epinephrine and neurologically favor- able survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA. 2013;310:270–279. doi: 10.1001/jama.2013.7832.
  218. Paris PM, Stewart RD, Deggler F. Prehospital use of dexamethasone in pulseless idioventricular rhythm. Ann Emerg Med. 1984;13:1008–1010.
  219. Tsai MS, Huang CH, Chang WT, Chen WJ, Hsu CY, Hsieh CC, Yang CW, Chiang WC, Ma MH, Chen SC. The effect of hydrocortisone on the outcome of out-of-hospital cardiac arrest patients: a pilot study. Am J Emerg Med. 2007;25:318–325. doi: 10.1016/j.ajem.2006.12.007.
  220. Wenzel V, Lindner KH, Krismer AC, Miller EA, Voelckel WG, Lingnau W. Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs. Circulation. 1999;99:1379–1384.
  221. Rittenberger JC, Menegazzi JJ, Callaway CW. Association of delay to first intervention with return of spontaneous circulation in a swine model of cardiac arrest. Resuscitation. 2007;73:154–160.
  222. Emerman CL, Pinchak AC, Hancock D, Hagen JF. The effect of bolus injection on circulation times during cardiac arrest. Am J Emerg Med. 1990;8:190–193.
  223. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseous route is a suitable alternative to intravenous route for fluid resuscitation in severely dehydrated children. Indian Pediatr. 1994;31:1511–1520.
  224. Brickman KR, Krupp K, Rega P, Alexander J, Guinness M. Typing and screening of blood from intraosseous access. Ann Emerg Med. 1992;21:414–417.
  225. Fiser RT, Walker WM, Seibert JJ, McCarthy R, Fiser DH. Tibial length following intraosseous infusion: a prospective, radiographic analysis. Pediatr Emerg Care. 1997;13:186–188.
  226. Ummenhofer W, Frei FJ, Urwyler A, Drewe J. Are laboratory values in bone marrow aspirate predictable for venous blood in paediatric patients? Resuscitation. 1994;27:123–128.
  227. Glaeser PW, Hellmich TR, Szewczuga D, Losek JD, Smith DS. Five-year experience in prehospital intraosseous infusions in children and adults. Ann Emerg Med. 1993;22:1119–1124.
  228. Guy J, Haley K, Zuspan SJ. Use of intraosseous infusion in the pediatric trauma patient. J Pediatr Surg. 1993;28:158–161.
  229. Macnab A, Christenson J, Findlay J, Horwood B, Johnson D, Jones L, Phillips K, Pollack C Jr., Robinson DJ, Rumball C, Stair T, Tiffany B, Whelan M. A new system for sternal intraosseous infusion in adults. Prehosp Emerg Care. 2000;4:173–177.
  230. Ellemunter H, Simma B, Trawoger R, Maurer H. Intraosseous lines in preterm and full term neonates. Arch Dis Child Fetal Neonatal Ed. 1999;80:F74–F75.
  231. Mader TJ, Kellogg AR, Walterscheid JK, Lodding CC, Sherman LD. A randomized comparison of cardiocerebral and cardiopulmonary resuscitation using a swine model of prolonged ventricular fibrillation. Resuscitation. 2010;81:596–602.
  232. Barsan WG, Levy RC, Weir H. Lidocaine levels during CPR: differences after peripheral venous, central venous, and intracardiac injections. Ann Emerg Med. 1981;10:73–78.
  233. Kuhn GJ, White BC, Swetnam RE, Mumey JF, Rydesky MF, Tintinalli JE, Krome RL, Hoehner PJ. Peripheral vs central circulation times during CPR: a pilot study. Ann Emerg Med. 1981;10:417–419.
  234. Emerman CL, Pinchak AC, Hancock D, Hagen JF. Effect of injection site on circulation times during cardiac arrest. Crit Care Med. 1988;16:1138–1141.
  235. Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M, Nowak RM. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA. 1990;263:1106–1113.
  236. Rivers EP, Martin GB, Smithline H, Rady MY, Schultz CH, Goetting MG, Appleton TJ, Nowak RM. The clinical implications of continuous central venous oxygen saturation during human CPR. Ann Emerg Med. 1992;21:1094–1101.
  237. Howard RF, Bingham RM. Endotracheal compared with intravenous administration of atropine. Arch Dis Child. 1990;65:449–450.
  238. Lee PL, Chung YT, Lee BY, Yeh CY, Lin SY, Chao CC. The optimal dose of atropine via the endotracheal route. Ma Zui Xue Za Zhi. 1989;27:35–38.
  239. Prengel AW, Lindner KH, Hahnel J, Ahnefeld FW. Endotracheal and endobronchial lidocaine administration: effects on plasma lidocaine concentration and blood gases. Crit Care Med. 1991;19:911–915.
  240. Schmidbauer S, Kneifel HA, Hallfeldt KK. Endobronchial application of high dose epinephrine in out of hospital cardiopulmonary resuscitation. Resuscitation. 2000;47:89.
  241. Raymondos K, Panning B, Leuwer M, Brechelt G, Korte T, Niehaus M, Tebbenjohanns J, Piepenbrock S. Absorption and hemodynamic effects of airway administration of adrenaline in patients with severe cardiac disease. Ann Intern Med. 2000;132:800–803.
  242. Hahnel JH, Lindner KH, Schurmann C, Prengel A, Ahnefeld FW. Plasma lidocaine levels and PaO2 with endobronchial administration: dilution with normal saline or distilled water? Ann Emerg Med. 1990;19:1314–1317.
  243. Brown LK, Diamond J. The efficacy of lidocaine in ventricular fibrillation due to coronary artery ligation: endotracheal vs intravenous use. Proc West Pharmacol Soc. 1982;25:43–45.
  244. Jasani MS, Nadkarni VM, Finkelstein MS, Hofmann WT, Salzman SK. Inspiratory-cycle instillation of endotracheal epinephrine in porcine arrest. Acad Emerg Med. 1994;1:340–345.
  245. Wenzel V, Lindner KH, Prengel AW, Lurie KG, Strohmenger HU. Endobronchial vasopressin improves survival during cardiopulmonary resuscitation in pigs. Anesthesiology. 1997;86:1375–1381.
  246. Prengel AW, Rembecki M, Wenzel V, Steinbach G. A comparison of the endotracheal tube and the laryngeal mask airway as a route for endobronchial lidocaine administration. Anesth Analg. 2001;92:1505–1509.
  247. Jasani MS, Nadkarni VM, Finkelstein MS, Mandell GA, Salzman SK, Norman ME. Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest. Crit Care Med. 1994;22:1174–1180.
  248. Johnston C. Endotracheal drug delivery. Pediatr Emerg Care. 1992;8:94–97.
  249. Efrati O, Ben-Abraham R, Barak A, Modan-Moses D, Augarten A, Manisterski Y, Barzilay Z, Paret G. Endobronchial adrenaline: should it be reconsidered? Dose response and haemodynamic effect in dogs. Resuscitation. 2003;59:117–122.
  250. Elizur A, Ben-Abraham R, Manisterski Y, Barak A, Efrati O, Lotan D, Barzilay Z, Paret G. Tracheal epinephrine or norepinephrine preceded by beta blockade in a dog model. Can beta blockade bestow any benefits? Resuscitation. 2003;59:271–276.
  251. Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Endotracheal drug administration during out-of-hospital resuscitation: where are the survivors? Resuscitation. 2002;53:153–157.
  252. Schuttler J, Bartsch A, Ebeling BJ, Hornchen U, Kulka P, Suhling B, Stoeckel H. [Endobronchial administration of adrenaline in preclinical cardiopulmonary resuscitation]. Anasth Intensivther Notfallmed. 1987;22:63–68.
  253. Hornchen U, Schuttler J, Stoeckel H, Eichelkraut W, Hahn N. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation. Crit Care Med. 1987;15:1037–1039.
  254. Naganobu K, Hasebe Y, Uchiyama Y, Hagio M, Ogawa H. A comparison of distilled water and normal saline as diluents for endobronchial administration of epinephrine in the dog. Anesth Analg. 2000;91:317–321.
  255. Ahrens T, Schallom L, Bettorf K, Ellner S, Hurt G, O’Mara V, Ludwig J, George W, Marino T, Shannon W. End-tidal carbon dioxide measure- ments as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care. 2001;10:391–398.
  256. Chen YS, Lin JW, Yu HY, Ko WJ, Jerng JS, Chang WT, Chen WJ, Huang SC, Chi NH, Wang CH, Chen LC, Tsai PR, Wang SS, Hwang JJ, Lin FY. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in- hospital cardiac arrest: an observational study and propensity analysis. Lancet. 2008;372:554–561. doi: 10.1016/S0140-6736(08)60958-7.
  257. Shin TG, Choi JH, Jo IJ, Sim MS, Song HG, Jeong YK, Song YB, Hahn JY, Choi SH, Gwon HC, Jeon ES, Sung K, Kim WS, Lee YT. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011;39:1–7. doi: 10.1097/CCM.0b013e3181feb339.
  258. Lin JW, Wang MJ, Yu HY, Wang CH, Chang WT, Jerng JS, Huang SC, Chou NK, Chi NH, Ko WJ, Wang YC, Wang SS, Hwang JJ, Lin FY, Chen YS. Comparing the survival between extracorporeal rescue and conventional resuscitation in adult in-hospital cardiac arrests: propen- sity analysis of three-year data. Resuscitation. 2010;81:796–803. doi: 10.1016/j.resuscitation.2010.03.002.
  259. Maekawa K, Tanno K, Hase M, Mori K, Asai Y. Extracorporeal cardio- pulmonary resuscitation for patients with out-of-hospital cardiac arrest of cardiac origin: a propensity-matched study and predictor analysis. Crit Care Med. 2013;41:1186–1196. doi: 10.1097/CCM.0b013e31827ca4c8.
  260. Sakamoto T, Morimura N, Nagao K, Asai Y, Yokota H, Nara S, Hase M, Tahara Y, Atsumi T; SAVE-J Study Group. Extracorporeal cardio- pulmonary resuscitation versus conventional cardiopulmonary resus- citation in adults with out-of-hospital cardiac arrest: a prospective observational study. Resuscitation. 2014;85:762–768. doi: 10.1016/j. resuscitation.2014.01.031.
  261. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest. JACEP. 1979;8:448–452.
  262. Sorensen M, Engbaek J, Viby-Mogensen J, Guldager H, Molke Jensen F. Bradycardia and cardiac asystole following a single injection of suxamethonium. Acta Anaesthesiol Scand. 1984;28:232–235.
  263. Lovstad RZ, Granhus G, Hetland S. Bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases. Acta Anaesthesiol Scand. 2000;44:48–52.
  264. Stueven HA, Tonsfeldt DJ, Thompson BM, Whitcomb J, Kastenson E, Aprahamian C. Atropine in asystole: human studies. Ann Emerg Med. 1984;13:815–817.
  265. Coon GA, Clinton JE, Ruiz E. Use of atropine for brady-asystolic prehospital cardiac arrest. Ann Emerg Med. 1981;10:462–467.
  266. Tortolani AJ, Risucci DA, Powell SR, Dixon R. In-hospital cardiopulmonary resuscitation during asystole. Therapeutic factors associated with 24-hour survival. Chest. 1989;96:622–626.
  267. Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN. Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs. Acad Emerg Med. 1995;2:264–273.
  268. Engdahl J, Bang A, Lindqvist J, Herlitz J. Can we define patients with no and those with some chance of survival when found in asystole out of hospital? Am J Cardiol. 2000;86:610–614.
  269. Engdahl J, Bang A, Lindqvist J, Herlitz J. Factors affecting short- and long-term prognosis among 1069 patients with out-of-hospital cardiac arrest and pulseless electrical activity. Resuscitation. 2001;51:17–25.
  270. van Walraven C, Stiell IG, Wells GA, Hebert PC, Vandemheen K. Do advanced cardiac life support drugs increase resuscitation rates from in-hospital cardiac arrest? The OTAC Study Group. Ann Emerg Med. 1998;32:544–553.
  271. Bar-Joseph G, Abramson NS, Kelsey SF, Mashiach T, Craig MT, Safar P. Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation. Acta Anaesthesiol Scand. 2005;49:6–15.
  272. Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb LA, Copass MK. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation. 1990;82:2027–2034.
  273. Dybvik T, Strand T, Steen PA. Buffer therapy during out-of-hospital cardiopulmonary resuscitation. Resuscitation. 1995;29:89–95.
  274. Vukmir RB, Katz L. Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest. Am J Emerg Med. 2006;24:156–161.
  275. Aufderheide TP, Martin DR, Olson DW, Aprahamian C, Woo JW, Hendley GE, Hargarten KM, Thompson B. Prehospital bicarbonate use in cardiac arrest: a 3-year experience. Am J Emerg Med. 1992;10:4–7.
  276. Skovron ML, Goldberg E, Suljaga-Petchel K. Factors predicting survival for six months after cardiopulmonary resuscitation: multivariate analysis of a prospective study. Mt Sinai J Med. 1985;52:271–275.
  277. Delooz HH, Lewi PJ. Are inter-center differences in EMS-management and sodium-bicarbonate administration important for the outcome of CPR? The Cerebral Resuscitation Study Group. Resuscitation. 1989; 17 suppl:S161–S172; discussion S199–S206.
  278. Roberts D, Landolfo K, Light R, Dobson K. Early predictors of mortality for hospitalized patients suffering cardiopulmonary arrest. Chest. 1990;97:413–419.
  279. Kette F, Weil MH, Gazmuri RJ. Buffer solutions may compromise cardiac resuscitation by reducing coronary perfusion presssure. JAMA. 1991;266:2121–2126.
  280. Graf H, Leach W, Arieff AI. Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science. 1985;227:754–756.
  281. Katz LM, Wang Y, Rockoff S, Bouldin TW. Low-dose Carbicarb improves cerebral outcome after asphyxial cardiac arrest in rats. Ann Emerg Med. 2002;39:359–365.
  282. Sun S, Weil MH, Tang W, Fukui M. Effects of buffer agents on postresuscitation myocardial dysfunction. Crit Care Med. 1996;24:2035–2041.
  283. Blecic S, De Backer D, Deleuze M, Vachiery JL, Vincent JL. Correction of metabolic acidosis in experimental CPR: a comparative study of sodium bicarbonate, carbicarb, and dextrose. Ann Emerg Med. 1991;20:235–238.
  284. Stueven HA, Thompson BM, Aprahamian C, Tonsfeldt DJ. Calcium chloride: reassessment of use in asystole. Ann Emerg Med. 1984;13:820–822.
  285. Stueven HA, Thompson B, Aprahamian C, Tonsfeldt DJ, Kastenson EH. The effectiveness of calcium chloride in refractory electromechanical dissociation. Ann Emerg Med. 1985;14:626–629.
  286. Stueven HA, Thompson B, Aprahamian C, Tonsfeldt DJ, Kastenson EH. Lack of effectiveness of calcium chloride in refractory asystole. Ann Emerg Med. 1985;14:630–632.
  287. Gando S, Tedo I, Tujinaga H, Kubota M. Variation in serum ionized calcium on cardiopulmonary resuscitation. J Anesth. 1988;2:154–160.
  288. Stueven H, Thompson BM, Aprahamian C, Darin JC. Use of calcium in prehospital cardiac arrest. Ann Emerg Med. 1983;12:136–139.
  289. Harrison EE, Amey BD. The use of calcium in cardiac resuscitation. Am J Emerg Med. 1983;1:267–273.
  290. Bottiger BW, Bode C, Kern S, Gries A, Gust R, Glatzer R, Bauer H, Motsch J, Martin E. Efficacy and safety of thrombolytic therapy after initially unsuccessful cardiopulmonary resuscitation: a prospective clinical trial. Lancet. 2001;357:1583–1585.
  291. Kurkciyan I, Meron G, Sterz F, Janata K, Domanovits H, Holzer M, Berzlanovich A, Bankl HC, Laggner AN. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160:1529–1535.
  292. Janata K, Holzer M, Kurkciyan I, Losert H, Riedmuller E, Pikula B, Laggner AN, Laczika K. Major bleeding complications in cardiopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism. Resuscitation. 2003;57:49–55.
  293. Lederer W, Lichtenberger C, Pechlaner C, Kroesen G, Baubin M. Recombinant tissue plasminogen activator during cardiopulmonary resuscitation in 108 patients with out-of-hospital cardiac arrest. Resuscitation. 2001;50:71–76.
  294. Bozeman WP, Kleiner DM, Ferguson KL. Empiric tenecteplase is associated with increased return of spontaneous circulation and short term survival in cardiac arrest patients unresponsive to standard interventions. Resuscitation. 2006;69:399–406.
  295. Stadlbauer KH, Krismer AC, Arntz HR, Mayr VD, Lienhart HG, Bottiger BW, Jahn B, Lindner KH, Wenzel V. Effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation. Am J Cardiol. 2006;97:305–308.
  296. Fatovich DM, Dobb GJ, Clugston RA. A pilot randomised trial of thrombolysis in cardiac arrest (the TICA trial). Resuscitation. 2004;61:309–313.
  297. Abu-Laban RB, Christenson JM, Innes GD, van Beek CA, Wanger KP, McKnight RD, MacPhail IA, Puskaric J, Sadowski RP, Singer J, Schechter MT, Wood VM. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346:1522–1528.
  298. Bender R, Breil M, Heister U, Dahmen A, Hoeft A, Krep H, Fischer M. Hypertonic saline during CPR: feasibility and safety of a new protocol of fluid management during resuscitation. Resuscitation. 2007;72:74–81.
  299. Breil M, Krep H, Sinn D, Hagendorff A, Dahmen A, Eichelkraut W, Hoeft A, Fischer M. Hypertonic saline improves myocardial blood flow during CPR, but is not enhanced further by the addition of hydroxy ethyl starch. Resuscitation. 2003;56:307–317.
  300. Bruel C, Parienti JJ, Marie W, Arrot X, Daubin C, Du Cheyron D, Massetti M, Charbonneau P. Mild hypothermia during advanced life support: a preliminary study in out-of-hospital cardiac arrest. Crit Care. 2008;12:R31.
  301. D'Alecy LG, Lundy EF, Barton KJ, Zelenock GB. Dextrose containing intravenous fluid impairs outcome and increases death after eight minutes of cardiac arrest and resuscitation in dogs. Surgery. 1986;100:505–511.
  302. Fischer M, Dahmen A, Standop J, Hagendorff A, Hoeft A, Krep H. Effects of hypertonic saline on myocardial blood flow in a porcine model of prolonged cardiac arrest. Resuscitation. 2002;54:269–280.
  303. Kamarainen A, Virkkunen I, Tenhunen J, Yli-Hankala A, Silfvast T. Prehospital induction of therapeutic hypothermia during CPR: a pilot study. Resuscitation. 2008;76:360–363.
  304. Krep H, Breil M, Sinn D, Hagendorff A, Hoeft A, Fischer M. Effects of hypertonic versus isotonic infusion therapy on regional cerebral blood flow after experimental cardiac arrest cardiopulmonary resuscitation in pigs. Resuscitation. 2004;63:73–83.
  305. Longstreth WT Jr., Copass MK, Dennis LK, Rauch-Matthews ME, Stark MS, Cobb LA. Intravenous glucose after out-of-hospital cardiopulmonary arrest: a community-based randomized trial. Neurology. 1993;43:2534–2541.
  306. Miclescu A, Basu S, Wiklund L. Methylene blue added to a hypertonic-hyperoncotic solution increases short-term survival in experimental cardiac arrest. Crit Care Med. 2006;34:2806–2813.
  307. Nordmark J, Rubertsson S. Induction of mild hypothermia with infusion of cold (4 degrees C) fluid during ongoing experimental CPR. Resuscitation. 2005;66:357–365.
  308. Nozari A, Safar P, Stezoski SW, Wu X, Kostelnik S, Radovsky A, Tisherman S, Kochanek PM. Critical time window for intra-arrest cooling with cold saline flush in a dog model of cardiopulmonary resuscitation. Circulation. 2006;113:2690–2696.
  309. Ujhelyi MR, Winecoff AP, Schur M, Frede T, Bottorff MB, Gabel M, Markel ML. Influence of hypertonic saline solution infusion on defibrillation efficacy. Chest. 1996;110:784–790.
  310. Ditchey RV, Lindenfeld J. Potential adverse effects of volume loading on perfusion of vital organs during closed-chest resuscitation. Circulation. 1984;69:181–189.
  311. Voorhees WD, Ralston SH, Kougias C, Schmitz PM. Fluid loading with whole blood or Ringer's lactate solution during CPR in dogs. Resuscitation. 1987;15:113–123.
  312. Yannopoulos D, Zviman M, Castro V, Kolandaivelu A, Ranjan R, Wilson RF, Halperin HR. Intra-cardiopulmonary resuscitation hypothermia with and without volume loading in an ischemic model of cardiac arrest. Circulation. 2009;120:1426–1435.
  313. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospital external cardiac pacing: a prospective, controlled clinical trial. Ann Emerg Med. 1988;17:1221–1226.
  314. Cummins RO, Graves JR, Larsen MP, Hallstrom AP, Hearne TR, Ciliberti J, Nicola RM, Horan S. Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac arrest. N Engl J Med. 1993;328:1377–1382.
  315. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B. Prehospital trial of emergency transcutaneous cardiac pacing. Circulation. 1987;76:1337–1343.
  316. White JD, Brown CG. Immediate transthoracic pacing for cardiac asystole in an emergency department setting. Am J Emerg Med. 1985;3:125–128.
  317. Haman L, Parizek P, Vojacek J. Precordial thump efficacy in termination of induced ventricular arrhythmias. Resuscitation. 2009;80:14–16.
  318. Pellis T, Kette F, Lovisa D, Franceschino E, Magagnin L, Mercante WP, Kohl P. Utility of pre-cordial thump for treatment of out of hospital cardiac arrest: a prospective study. Resuscitation. 2009;80:17–23.
  319. Befeler B. Mechanical stimulation of the heart: its therapeutic value in tachyarrhythmias. Chest. 1978;73:832–838.
  320. Volkmann H, Klumbies A, Kuhnert H, Paliege R, Dannberg G, Siegert K. [Terminating ventricular tachycardias by mechanical heart stimulation with precordial thumps]. Z Kardiol. 1990;79:717–724.
  321. Caldwell G, Millar G, Quinn E, Vincent R, Chamberlain DA. Simple mechanical methods for cardioversion: defence of the precordial thump and cough version. BMJ (Clin Res Ed). 1985;291:627–630.
  322. Morgera T, Baldi N, Chersevani D, Medugno G, Camerini F. Chest thump and ventricular tachycardia. Pacing Clin Electrophysiol. 1979;2:69–75.
  323. Rahner E, Zeh E. Die Regularisierung von Kammertachykardien durch präkordialen Faustschlag. [Regulation of ventricular tachycardia with precordial fist blow]. Med Welt. 1978;29:1659–1663.
  324. Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease. Clin Cardiol. 1992;15:181–188.
  325. Krijne R. Rate acceleration of ventricular tachycardia after a precordial chest thump. Am J Cardiol. 1984;53:964–965.
  326. Sclarovsky S, Kracoff OH, Agmon J. Acceleration of ventricular tachycardia induced by a chest thump. Chest. 1981;80:596–599.
  327. Yakaitis RW, Redding JS. Precordial thumping during cardiac resuscitation. Crit Care Med. 1973;1:22–26.
  328. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112(24 suppl):IV1–IV203.
  329. Smith I, Monk TG, White PF. Comparison of transesophageal atrial pacing with anticholinergic drugs for the treatment of intraoperative bradycardia. Anesth Analg. 1994;78:245–252.
  330. Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations. Resuscitation. 1999;41:47–55.
  331. Swart G, Brady WJJ, DeBehnke DJ, John OM, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine. Am J Emerg Med. 1999;17:647–652.
  332. Chadda KD, Lichstein E, Gupta PK, Choy R. Bradycardia-hypotension syndrome in acute myocardial infarction. Reappraisal of the overdrive effects of atropine. Am J Med. 1975;59:158–164.
  333. Chadda KD, Lichstein E, Gupta PK, Kourtesis P. Effects of atropine in patients with bradyarrhythmia complicating myocardial infarction: usefulness of an optimum dose for overdrive. Am J Med. 1977;63:503–510.
  334. Dauchot P, Gravenstein JS. Effects of atropine on the electrocardiogram in different age groups. Clin Pharmacol Ther. 1971;12:274–280.
  335. Bernheim A, Fatio R, Kiowski W, Weilenmann D, Rickli H, Rocca HP. Atropine often results in complete atrioventricular block or sinus arrest after cardiac transplantation: an unpredictable and dose-independent phenomenon. Transplantation. 2004;77:1181–1185.
  336. Morrison LJ, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, Cameron B, Burgess R, Shield J, Bagley P, Mausz V, Brewer JE, Dorian P. A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: ‘PrePACE.’ Resuscitation. 2008;76:341–349.
  337. Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J. 1967;29:469–489.
  338. Mittal S, Ayati S, Stein KM, Schwartzman D, Cavlovich D, Tchou PJ, Markowitz SM, Slotwiner DJ, Scheiner MA, Lerman BB. Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation. 2000;101:1282–1287.
  339. Page RL, Kerber RE, Russell JK, Trouton T, Waktare J, Gallik D, Olgin JE, Ricard P, Dalzell GW, Reddy R, Lazzara R, Lee K, Carlson M, Halperin B, Bardy GH. Biphasic versus monophasic shock waveform for conversion of atrial fibrillation: the results of an international randomized, double-blind multicenter trial. J Am Coll Cardiol. 2002;39:1956–1963.
  340. Scholten M, Szili-Torok T, Klootwijk P, Jordaens L. Comparison of monophasic and biphasic shocks for transthoracic cardioversion of atrial fibrillation. Heart. 2003;89:1032–1034.
  341. Glover BM, Walsh SJ, McCann CJ, Moore MJ, Manoharan G, Dalzell GW, McAllister A, McClements B, McEneaney DJ, Trouton TG, Mathew TP, Adgey AA. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial. Heart. 2008;94:884–887.
  342. Reisinger J, Gstrein C, Winter T, Zeindlhofer E, Hollinger K, Mori M, Schiller A, Winter A, Geiger H, Siostrzonek P. Optimization of initial energy for cardioversion of atrial tachyarrhythmias with biphasic shocks. Am J Emerg Med. 2010;28:159–165.
  343. Kerber RE, Martins JB, Kienzle MG, Constantin L, Olshansky B, Hopson R, Charbonnier F. Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment. Circulation. 1988;77:1038–1046.
  344. Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998;31:30–35.
  345. Wen ZC, Chen SA, Tai CT, Chiang CE, Chiou CW, Chang MS. Electrophysiological mechanisms and determinants of vagal maneuvers for termination of paroxysmal supraventricular tachycardia. Circulation. 1998;98:2716–2723.
  346. Ornato JP, Hallagan LF, Reese WA, Clark RF, Tayal VS, Garnett AR, Gonzalez ER. Treatment of paroxysmal supraventricular tachycardia in the emergency department by clinical decision analysis. Am J Emerg Med. 1988;6:555–560.
  347. DiMarco JP, Miles W, Akhtar M, Milstein S, Sharma AD, Platia E, McGovern B, Scheinman MM, Govier WC. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil: assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group [published correction appears in Ann Intern Med. 1990;113:996]. Ann Intern Med. 1990;113:104–110.
  348. Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80:523–528.
  349. Cheng KA. [A randomized, multicenter trial to compare the safety and efficacy of adenosine versus verapamil for termination of paroxysmal supraventricular tachycardia]. Zhonghua Nei Ke Za Zhi. 2003;42:773–776.
  350. Hood MA, Smith WM. Adenosine versus verapamil in the treatment of supraventricular tachycardia: a randomized double-crossover trial. Am Heart J. 1992;123:1543–1549.
  351. Rankin AC, Oldroyd KG, Chong E, Dow JW, Rae AP, Cobbe SM. Adenosine or adenosine triphosphate for supraventricular tachycardias? Comparative double-blind randomized study in patients with spontaneous or inducible arrhythmias. Am Heart J. 1990;119:316–323.
  352. Brady WJ Jr., DeBehnke DJ, Wickman LL, Lindbeck G. Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil. Acad Emerg Med. 1996;3:574–585.
  353. Morrison LJ, Allan R, Vermeulen M, Dong SL, McCallum AL. Conversion rates for prehospital paroxysmal supraventricular tachycardia (PSVT) with the addition of adenosine: a before-and-after trial. Prehosp Emerg Care. 2001;5:353–359.
  354. Glatter K, Cheng J, Dorostkar P, Modin G, Talwar S, Al-Nimri M, Lee R, Saxon L, Lesh M, Scheinman M. Electrophysiologic effects of adenosine in patients with supraventricular tachycardia. Circulation. 1999;99:1034–1040.
  355. Cairns CB, Niemann JT. Intravenous adenosine in the emergency department management of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1991;20:717–721.
  356. Davis R, Spitalnic SJ, Jagminas L. Cost-effective adenosine dosing for the treatment of PSVT. Am J Emerg Med. 1999;17:633–634.
  357. Gausche M, Persse DE, Sugarman T, Shea SR, Palmer GL, Lewis RJ, Brueske PJ, Mahadevan S, Melio FR, Kuwata JH, Niemann JT. Adenosine for the prehospital treatment of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1994;24:183–189.
  358. McIntosh-Yellin NL, Drew BJ, Scheinman MM. Safety and efficacy of central intravenous bolus administration of adenosine for termination of supraventricular tachycardia. J Am Coll Cardiol. 1993;22:741–745.
  359. Riccardi A, Arboscello E, Ghinatti M, Minuto P, Lerza R. Adenosine in the treatment of supraventricular tachycardia: 5 years of experience (2002–2006). Am J Emerg Med. 2008;26:879–882.
  360. Sellers TD, Kirchhoffer JB, Modesto TA. Adenosine: a clinical experience and comparison with verapamil for the termination of supraventricular tachycardias. Prog Clin Biol Res. 1987;230:283–299.
  361. Marco CA, Cardinale JF. Adenosine for the treatment of supraventricular tachycardia in the ED. Am J Emerg Med. 1994;12:485–488.
  362. Seet CM. Efficacy of intravenous adenosine in treatment of paroxysmal supraventricular tachycardia in the local population. Singapore Med J. 1997;38:525–528.
  363. Tan H, Spekhorst H, Peters R, Wilde A. Adenosine induced ventricular arrhythmias in the emergency room. Pacing Clin Electrophysiol. 2001;24:450–455.
  364. Madsen CD, Pointer JE, Lynch TG. A comparison of adenosine and verapamil for the treatment of supraventricular tachycardia in the prehospital setting. Ann Emerg Med. 1995;25:649–655.
  365. Cybulski J, Kulakowski P, Makowska E, Czepiel A, Sikora-Frac M, Ceremuzynski L. Intravenous amiodarone is safe and seems to be effective in termination of paroxysmal supraventricular tachyarrhythmias. Clin Cardiol. 1996;19:563–566.
  366. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol. 2003;88:129–133.
  367. Camm AJ, Garratt CJ. Adenosine and supraventricular tachycardia. N Engl J Med. 1991;325:1621–1629.
  368. Lim SH, Anantharaman V, Teo WS. Slow-infusion of calcium channel blockers in the emergency management of supraventricular tachycardia. Resuscitation. 2002;52:167–174.
  369. Ferreira JF, Pamplona D, Cesar LA, Leite PF, Sosa EA, da Luz PL, Bellotti G. [Comparative study between verapamil and adenosine triphosphate in the treatment of paroxysmal supraventricular tachycardia]. Arq Bras Cardiol. 1996;66:55–57.
  370. Rankin AC, Rae AP, Oldroyd KG, Cobbe SM. Verapamil or adenosine for the immediate treatment of supraventricular tachycardia. Q J Med. 1990;74:203–208.
  371. Joshi PP, Deshmukh PK, Salkar RG. Efficacy of intravenous magnesium sulphate in supraventricular tachyarrhythmias. J Assoc Physicians India. 1995;43:529–531.
  372. Gupta A, Naik A, Vora A, Lokhandwala Y. Comparison of efficacy of intravenous diltiazem and esmolol in terminating supraventricular tachycardia. J Assoc Physicians India. 1999;47:969–972.
  373. Boudonas G, Lefkos N, Efthymiadis AP, Styliadis IG, Tsapas G. Intravenous administration of diltiazem in the treatment of supraventricular tachyarrhythmias. Acta Cardiol. 1995;50:125–134.
  374. Staudinger T, Brugger S, Roggla M, Rintelen C, Atherton GL, Johnson JC, Frass M. [Comparison of the Combitube with the endotracheal tube in cardiopulmonary resuscitation in the prehospital phase]. Wien Klin Wochenschr. 1994;106:412–415.
  375. Marill KA, Wolfram S, Desouza IS, Nishijima DK, Kay D, Setnik GS, Stair TO, Ellinor PT. Adenosine for wide-complex tachycardia: efficacy and safety. Crit Care Med. 2009;37:2512–2518.
  376. Domanovits H, Laske H, Stark G, Sterz F, Schmidinger H, Schreiber W, Mullner M, Laggner AN. Adenosine for the management of patients with tachycardias—a new protocol. Eur Heart J. 1994;15:589–593.
  377. Ilkhanipour K, Berrol R, Yealy DM. Therapeutic and diagnostic efficacy of adenosine in wide-complex tachycardia. Ann Emerg Med. 1993;22:1360–1364.
  378. Rankin AC, Oldroyd KG, Chong E, Rae AP, Cobbe SM. Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br Heart J. 1989;62:195–203.
  379. Wilber DJ, Baerman J, Olshansky B, Kall J, Kopp D. Adenosine-sensitive ventricular tachycardia. Clinical characteristics and response to catheter ablation. Circulation. 1993;87:126–134.
  380. Armengol RE, Graff J, Baerman JM, Swiryn S. Lack of effectiveness of lidocaine for sustained, wide QRS complex tachycardia. Ann Emerg Med. 1989;18:254–257.
  381. Exner DV, Muzyka T, Gillis AM. Proarrhythmia in patients with the Wolff-Parkinson-White syndrome after standard doses of intravenous adenosine. Ann Intern Med. 1995;122:351–352.
  382. Gupta AK, Shah CP, Maheshwari A, Thakur RK, Hayes OW, Lokhandwala YY. Adenosine induced ventricular fibrillation in Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol. 2002;25:477–480.
  383. Shah CP, Gupta AK, Thakur RK, Hayes OW, Mehrotra A, Lokhandwala YY. Adenosine-induced ventricular fibrillation. Indian Heart J. 2001;53:208–210.
  384. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Case report: adenosine induced ventricular fibrillation in a patient with stable ventricular tachycardia. J Interv Card Electrophysiol. 2001;5:71–74.
  385. Buxton AE, Marchlinski FE, Doherty JU, Flores B, Josephson ME. Hazards of intravenous verapamil for sustained ventricular tachycardia. Am J Cardiol. 1987;59:1107–1110.
  386. Gorgels AP, van den Dool A, Hofs A, Mulleneers R, Smeets JL, Vos MA, Wellens HJ. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol. 1996;78:43–46.
  387. Ho DS, Zecchin RP, Richards DA, Uther JB, Ross DL. Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet. 1994;344:18–23.
  388. Ho DSW, Zecchin RP, Cooper MJ, Richards DAB, Uther JB, Ross DL. Rapid intravenous infusion of d-1 sotalol: time to onset of effects on ventricular refractoriness, and safety. Eur Heart J. 1995;16:81–86.
  389. Somberg JC, Bailin SJ, Haffajee CI, Paladino WP, Kerin NZ, Bridges D, Timar S, Molnar J. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol. 2002;90:853–859.
  390. Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med. 2006;47:217–224.
  391. Schutzenberger W, Leisch F, Kerschner K, Harringer W, Herbinger W. Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation. Br Heart J. 1989;62:367–371.
  392. Tomlinson DR, Cherian P, Betts TR, Bashir Y. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J. 2008;25:15–18.
  393. Nasir N Jr., Taylor A, Doyle TK, Pacifico A. Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction. Am J Cardiol. 1994;74:1183–1186.
  394. Marill KA, Greenberg GM, Kay D, Nelson BK. Analysis of the treatment of spontaneous sustained stable ventricular tachycardia. Acad Emerg Med. 1997;4:1122–1128.
  395. Koster RW, Dunning AJ. Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospitalization phase of acute myocardial infarction. N Engl J Med. 1985;313:1105–1110.
  396. Roth A, Malov N, Bloch Y, Schlesinger Z, Laniado S, Kaplinski E. Usefulness of self-administration of intramuscular lidocaine in the prehospital setting for ventricular tachyarrhythmias unassociated with acute myocardial infarction (The “SHAHAL” experience in Israel). Am J Cardiol. 1997;79:611–614.
  397. Fuster V, Ryden LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey JY, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S, Smith SC Jr., Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114:e257–e354.
  398. Sticherling C, Tada H, Hsu W, Bares AC, Oral H, Pelosi F, Knight BP, Strickberger SA, Morady F. Effects of diltiazem and esmolol on cycle length and spontaneous conversion of atrial fibrillation. J Cardiovasc Pharmacol Ther. 2002;7:81–88.
  399. Chiladakis JA, Stathopoulos C, Davlouros P, Manolis AS. Intravenous magnesium sulfate versus diltiazem in paroxysmal atrial fibrillation. Int J Cardiol. 2001;79:287–291.
  400. Schreck DM, Rivera AR, Tricarico VJ. Emergency management of atrial fibrillation and flutter: intravenous diltiazem versus intravenous digoxin. Ann Emerg Med. 1997;29:135–140.
  401. Siu CW, Lau CP, Lee WL, Lam KF, Tse HF. Intravenous diltiazem is superior to intravenous amiodarone or digoxin for achieving ventricular rate control in patients with acute uncomplicated atrial fibrillation. Crit Care Med. 2009;37:2174–2179, quiz 2180.
  402. Intravenous digoxin in acute atrial fibrillation. Results of a randomized, placebo-controlled multicentre trial in 239 patients. The Digitalis in Acute Atrial Fibrillation (DAAF) Trial Group. Eur Heart J. 1997;18:649–654.
  403. Jordaens L, Trouerbach J, Calle P, Tavernier R, Derycke E, Vertongen P, Bergez B, Vandekerckhove Y. Conversion of atrial fibrillation to sinus rhythm and rate control by digoxin in comparison to placebo. Eur Heart J. 1997;18:643–648.
  404. Wattanasuwan N, Khan IA, Mehta NJ, Arora P, Singh N, Vasavada BC, Sacchi TJ. Acute ventricular rate control in atrial fibrillation: IV combination of diltiazem and digoxin vs IV diltiazem alone. Chest. 2001;119:502–506.
  405. Galve E, Rius T, Ballester R, Artaza MA, Arnau JM, Garcia-Dorado D, Soler-Soler J. Intravenous amiodarone in treatment of recent-onset atrial fibrillation: results of a randomized, controlled study. J Am Coll Cardiol. 1996;27:1079–1082.
  406. Thomas SP, Guy D, Wallace E, Crampton R, Kijvanit P, Eipper V, Ross DL, Cooper MJ. Rapid loading of sotalol or amiodarone for management of recent onset symptomatic atrial fibrillation: a randomized, digoxin-controlled trial. Am Heart J. 2004;147:E3.
  407. Kramer-Johansen J, Wik L, Steen PA. Advanced cardiac life support before and after tracheal intubation—direct measurements of quality. Resuscitation. 2006;68:61–69.
  408. Cantineau JP, Lambert Y, Merckx P, Reynaud P, Porte F, Bertrand C, Duvaldestin P. End-tidal carbon dioxide during cardiopulmonary resuscitation in humans presenting mostly with asystole: a predictor of outcome. Crit Care Med. 1996;24:791–796.
  409. Keren A, Tzivoni D, Gavish D, Levi J, Gottlieb S, Benhorin J, Stern S. Etiology, warning signs and therapy of torsade de pointes: a study of 10 patients. Circulation. 1981;64:1167–1174.
  410. Nguyen PT, Scheinman MM, Seger J. Polymorphous ventricular tachycardia: clinical characterization, therapy, and the QT interval. Circulation. 1986;74:340–349.
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Part 7: Adult Advanced Cardiovascular Life Support