Cardiopulmonary Resuscitation (CPR)



Cardiopulmonary Resuscitation (CPR)

Red Cross CPR Steps    CPR: First aid (Mayo Clinic)    American Heart Association Guidelines    Medications    Bradycardia/Tachycardia    CPR in Adults (Merck Manual)    Summary   

Red Cross CPR Steps

Cardiopulmonary resuscitation (CPR) can help save a life during a cardiac or breathing emergency. However, even after training, remembering the CPR steps and administering them correctly can be a challenge. In order to help you help someone in need, we've created this simple step-by-step guide that you can print up and place on your refrigerator, in your car, in your bag or at your desk.

Before Giving CPR

1 Check the scene and the person. Make sure the scene is safe, then tap the person on the shoulder and shout "Are you OK?" to ensure that the person needs help.

2 Call 911 for assistance. If it's evident that the person needs help, call (or ask a bystander to call) 911, then send someone to get an AED. (If an AED is unavailable, or a there is no bystander to access it, stay with the victim, call 911 and begin administering assistance.)

3 Open the airway. With the person lying on his or her back, tilt the head back slightly to lift the chin.

4 Check for breathing. Listen carefully, for no more than 10 seconds, for sounds of breathing. (Occasional gasping sounds do not equate to breathing.) If there is no breathing begin CPR.

Red Cross CPR Steps

1 Push hard, push fast. Place your hands, one on top of the other, in the middle of the chest. Use your body weight to help you administer compressions that are at least 2 inches deep and delivered at a rate of at least 100 compressions per minute.

2 Deliver rescue breaths. With the person's head tilted back slightly and the chin lifted, pinch the nose shut and place your mouth over the person's mouth to make a complete seal. Blow into the person's mouth to make the chest rise. Deliver two rescue breaths, then continue compressions.

Note: If the chest does not rise with the initial rescue breath, re-tilt the head before delivering the second breath. If the chest doesn't rise with the second breath, the person may be choking. After each subsequent set of 100 chest compressions, and before attempting breaths, look for an object and, if seen, remove it.

3 Continue CPR steps. Keep performing cycles of chest compressions and breathing until the person exhibits signs of life, such as breathing, an AED becomes available, or EMS or a trained medical responder arrives on scene.

Note: End the cycles if the scene becomes unsafe or you cannot continue performing CPR due to exhaustion.

To see the steps to perform CPR in action, watch our video Putting it All Together: CPR – Adult. Or, for online, in person and blended training courses, visit our CPR Training Page.

 

 

Cardiopulmonary resuscitation (CPR): First aid (Mayo Clinic)

Cardiopulmonary resuscitation (CPR) is a lifesaving technique useful in many emergencies, including a heart attack or near drowning, in which someone's breathing or heartbeat has stopped. The American Heart Association recommends that everyone — untrained bystanders and medical personnel alike — begin CPR with chest compressions.

It's far better to do something than to do nothing at all if you're fearful that your knowledge or abilities aren't 100 percent complete. Remember, the difference between your doing something and doing nothing could be someone's life.

Here's advice from the American Heart Association:
Untrained. If you're not trained in CPR, then provide hands-only CPR. That means uninterrupted chest compressions of 100 to 120 a minute until paramedics arrive (described in more detail below). You don't need to try rescue breathing.
Trained and ready to go. If you're well-trained and confident in your ability, check to see if there is a pulse and breathing. If there is no breathing or a pulse within 10 seconds, begin chest compressions. Start CPR with 30 chest compressions before giving two rescue breaths.
Trained but rusty. If you've previously received CPR training but you're not confident in your abilities, then just do chest compressions at a rate of 100 to 120 a minute. (Details described below.)

The above advice applies to adults, children and infants needing CPR, but not newborns (infants up to 4 weeks old).

CPR can keep oxygenated blood flowing to the brain and other vital organs until more definitive medical treatment can restore a normal heart rhythm.

When the heart stops, the lack of oxygenated blood can cause brain damage in only a few minutes. A person may die within eight to 10 minutes.

To learn CPR properly, take an accredited first-aid training course, including CPR and how to use an automated external defibrillator (AED). If you are untrained and have immediate access to a phone, call 911 or your local emergency number before beginning CPR. The dispatcher can instruct you in the proper procedures until help arrives.

Before you begin

Before starting CPR, check:
• Is the environment safe for the person?
• Is the person conscious or unconscious?
• If the person appears unconscious, tap or shake his or her shoulder and ask loudly, "Are you OK?"
• If the person doesn't respond and two people are available, have one person call 911 or the local emergency number and get the AED, if one is available, and have the other person begin CPR.
• If you are alone and have immediate access to a telephone, call 911 or your local emergency number before beginning CPR. Get the AED, if one is available.
• As soon as an AED is available, deliver one shock if instructed by the device, then begin CPR.

Remember to spell C-A-B

The American Heart Association uses the letters C-A-B — compressions, airway, breathing — to help people remember the order to perform the steps of CPR.

Compressions: Restore blood circulation
1. Put the person on his or her back on a firm surface.
2. Kneel next to the person's neck and shoulders.
3. Place the heel of one hand over the center of the person's chest, between the nipples. Place your other hand on top of the first hand. Keep your elbows straight and position your shoulders directly above your hands.
4. Use your upper body weight (not just your arms) as you push straight down on (compress) the chest at least 2 inches (approximately 5 centimeters) but not greater than 2.4 inches (approximately 6 centimeters). Push hard at a rate of 100 to 120 compressions a minute.
5. If you haven't been trained in CPR, continue chest compressions until there are signs of movement or until emergency medical personnel take over. If you have been trained in CPR, go on to opening the airway and rescue breathing.

Airway: Open the airway
• If you're trained in CPR and you've performed 30 chest compressions, open the person's airway using the head-tilt, chin-lift maneuver. Put your palm on the person's forehead and gently tilt the head back. Then with the other hand, gently lift the chin forward to open the airway.

Breathing: Breathe for the person
Rescue breathing can be mouth-to-mouth breathing or mouth-to-nose breathing if the mouth is seriously injured or can't be opened.
1. With the airway open (using the head-tilt, chin-lift maneuver), pinch the nostrils shut for mouth-to-mouth breathing and cover the person's mouth with yours, making a seal.
2. Prepare to give two rescue breaths. Give the first rescue breath — lasting one second — and watch to see if the chest rises. If it does rise, give the second breath. If the chest doesn't rise, repeat the head-tilt, chin-lift maneuver and then give the second breath. Thirty chest compressions followed by two rescue breaths is considered one cycle. Be careful not to provide too many breaths or to breathe with too much force.
3. Resume chest compressions to restore circulation.
4. As soon as an automated external defibrillator (AED) is available, apply it and follow the prompts. Administer one shock, then resume CPR — starting with chest compressions — for two more minutes before administering a second shock. If you're not trained to use an AED, a 911 or other emergency medical operator may be able to guide you in its use. If an AED isn't available, go to step 5 below.
5. Continue CPR until there are signs of movement or emergency medical personnel take over.

To perform CPR on a child

The procedure for giving CPR to a child age 1 through puberty is essentially the same as that for an adult. The American Heart Association also recommends the following to perform CPR on a child:

Compressions: Restore blood circulation

If you are alone and didn't see the child collapse, perform five cycles of compressions and breaths on the child — this should take about two minutes — before calling 911 or your local emergency number and getting the AED, if one is available.

If you're alone and you did see the child collapse, call 911 or your local emergency number and get the AED, if one is available, before beginning CPR. If another person is available, have that person call for help and get the AED while you begin CPR.
1. Put the child on his or her back on a firm surface.
2. Kneel next to the child's neck and shoulders.
3. Use two hands, or only one hand if the child is very small, to perform chest compressions. Press straight down on (compress) the chest about 2 inches (approximately 5 centimeters). If the child is an adolescent, push straight down on the chest at least 2 inches (approximately 5 centimeters) but not greater than 2.4 inches (approximately 6 centimeters). Push hard at a rate of 100 to 120 compressions a minute.
4. If you haven't been trained in CPR, continue chest compressions until there are signs of movement or until emergency medical personnel take over. If you have been trained in CPR, go on to opening the airway and rescue breathing.

Airway: Open the airway

• If you're trained in CPR and you've performed 30 chest compressions, open the child's airway using the head-tilt, chin-lift maneuver. Put your palm on the child's forehead and gently tilt the head back. Then with the other hand, gently lift the chin forward to open the airway.

Breathing: Breathe for the child

Use the same compression-breath rate that is used for adults: 30 compressions followed by two breaths. This is one cycle.
1. With the airway open (using the head-tilt, chin-lift maneuver), pinch the nostrils shut for mouth-to-mouth breathing and cover the child's mouth with yours, making a seal.
2. Prepare to give two rescue breaths. Give the first rescue breath — lasting one second — and watch to see if the chest rises. If it does rise, give the second breath. If the chest doesn't rise, repeat the head-tilt, chin-lift maneuver and then give the second breath. Be careful not to provide too many breaths or to breathe with too much force.
3. After the two breaths, immediately begin the next cycle of compressions and breaths. If there are two people performing CPR, conduct 15 compressions followed by two breaths.
4. As soon as an AED is available, apply it and follow the prompts. Use pediatric pads if available, for children up to age 8. If pediatric pads aren't available, use adult pads. Administer one shock, then resume CPR — starting with chest compressions — for two more minutes before administering a second shock. If you're not trained to use an AED, a 911 or other emergency medical operator may be able to guide you in its use.

Continue until the child moves or help arrives.

To perform CPR on a baby 4 weeks old and older

Most cardiac arrests in babies occur from lack of oxygen, such as from drowning or choking. If you know the baby has an airway obstruction, perform first aid for choking. If you don't know why the baby isn't breathing, perform CPR.

To begin, examine the situation. Stroke the baby and watch for a response, such as movement, but don't shake the baby.

If there's no response, follow the C-A-B procedures below for a baby under age 1 (except newborns, which includes babies up to 4 weeks old) and time the call for help as follows:
• If you're the only rescuer and you didn't see the baby collapse, do CPR for two minutes — about five cycles — before calling 911 or your local emergency number and getting the AED. If you did see the baby collapse, call 911 or your local emergency number and get the AED, if one is available, before beginning CPR.
• If another person is available, have that person call for help immediately and get the AED while you attend to the baby.

Compressions: Restore blood circulation
1. Place the baby on his or her back on a firm, flat surface, such as a table. The floor or ground also will do.
2. Imagine a horizontal line drawn between the baby's nipples. Place two fingers of one hand just below this line, in the center of the chest.
3. Gently compress the chest about 1.5 inches (about 4 centimeters).
4. Count aloud as you pump in a fairly rapid rhythm. You should pump at a rate of 100 to 120 compressions a minute.

Airway: Open the airway
• After 30 compressions, gently tip the head back by lifting the chin with one hand and pushing down on the forehead with the other hand.

Breathing: Breathe for the baby
1. Cover the baby's mouth and nose with your mouth.
2. Prepare to give two rescue breaths. Use the strength of your cheeks to deliver gentle puffs of air (instead of deep breaths from your lungs) to slowly breathe into the baby's mouth one time, taking one second for the breath. Watch to see if the baby's chest rises. If it does, give a second rescue breath. If the chest does not rise, repeat the head-tilt, chin-lift maneuver and then give the second breath.
3. If the baby's chest still doesn't rise, continue chest compressions.
4. Give two breaths after every 30 chest compressions. If two people are conducting CPR, give two breaths after every 15 chest compressions.
5. Perform CPR for about two minutes before calling for help unless someone else can make the call while you attend to the infant.
6. Continue CPR until you see signs of life or until medical personnel arrive.

 

 

American Heart Association Guidelines for
Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC)

 

2017 (Updated):

• Dispatch-assisted CPR
We recommend that when dispatchers’ instructions are needed, dispatchers should provide chest compression–only CPR instructions to callers for adults with suspected out-of-hospital cardiac arrest (OHCA).

• Bystander CPR
1. For adults in OHCA, untrained lay rescuers should provide chest compression–only CPR with or without dispatcher assistance.
2. For lay rescuers trained in chest compression–only CPR, we recommend that they provide chest compression–only CPR for adults in OHCA.
3. For lay rescuers trained in CPR using chest compressions and ventilation (rescue breaths), it is reasonable to provide ventilation (rescue breaths) in addition to chest compressions for the adult in OHCA.

• EMS-Delivered CPR 1. We recommend that before placement of an advanced airway (supraglottic airway or tracheal tube), EMS providers perform CPR with cycles of 30 compressions and 2 breaths. As an alternative, it is reasonable for EMS providers to perform CPR in cycles of 30 compressions and 2 breaths without interrupting chest compressions to give breaths. It may be reasonable for EMS providers to use a rate of 10 breaths per minute (1 breath every 6 seconds) to provide asynchronous ventilation during continuous chest compressions before placement of an advanced airway.
2. These updated recommendations do not preclude the 2015 recommendation that a reasonable alternative for EMS systems that have adopted bundles of care is the initial use of minimally interrupted chest compressions (ie, delayed ventilation) for witnessed, shockable OHCA.

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

Pediatric BLS and CPR Quality
• Reaffirming that compressions and ventilation are needed for infants and children in cardiac arrest
• Strongly recommending that bystanders who are unwilling or unable to deliver rescue breaths should provide chest compressions for infants and children

Chest Compression Depth
2015 (Updated):
During manual CPR, rescuers should perform chest compressions to a depth of at least 2 inches (5 cm) for an average adult, while avoiding excessive chest compression depths (greater than 2.4 inches [6 cm]).

2015 (Updated):

Adult Basic Life Support and CPR Quality: Lay Rescuer CPR
• The recommended sequence for a single rescuer has been confirmed: the single rescuer is to initiate chest compressions before giving rescue breaths (C-A-B rather than A-B-C) to reduce delay to first compression. The single rescuer should begin CPR with 30 chest compressions followed by 2 breaths.
• There is continued emphasis on the characteristics of high-quality CPR: compressing the chest at an adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in compressions, and avoiding excessive ventilation.
• The recommended chest compression rate is 100 to 120/min (updated from at least 100/min).
• The clarified recommendation for chest compression depth for adults is at least 2 inches (5 cm) but not greater than 2.4 inches (6 cm).
• Bystander-administered naloxone may be considered for suspected life-threatening opioid-associated emergencies. (Administer naloxone: Give naloxone 2 mg intranasal or 0.4 mg intramuscular. May repeat after 4 minutes.)

These changes are designed to simplify lay rescuer training and to emphasize the need for early chest compressions for victims of sudden cardiac arrest.

Emphasis on Chest Compressions
Untrained lay rescuers should provide compression-only (Hands-Only) CPR, with or without dispatcher guidance, for adult victims of cardiac arrest. The rescuer should continue compression-only CPR until the arrival of an AED or rescuers with additional training. All lay rescuers should, at a minimum, provide chest compressions for victims of cardiac arrest. In addition, if the trained lay rescuer is able to perform rescue breaths, he or she should add rescue breaths in a ratio of 30 compressions to 2 breaths. The rescuer should continue CPR until an AED arrives and is ready for use, EMS providers take over care of the victim, or the victim starts to move.

Chest Compression Rate
In adult victims of cardiac arrest, it is reasonable for rescuers to perform chest compressions at a rate of 100 to 120/min.

Chest Compression Rate
During manual CPR, rescuers should perform chest compressions to a depth of at least 2 inches (5 cm) for an average adult, while avoiding excessive chest compression depths (greater than 2.4 inches [6 cm]).

Adult Basic Life Support and CPR Quality: HCP BL
• Trained rescuers are encouraged to simultaneously perform some steps (ie, checking for breathing and pulse at the same time), in an effort to reduce the time to first chest compression.

• For patients with ongoing CPR and an advanced airway in place, a simplified ventilation rate of 1 breath every 6 seconds (10 breaths per minute) is recommended.

 



Adult Advanced Cardiovascular Life Support

Web-based Integrated 2010 & 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care


1. Highlights
2. Introduction
3. Adjuncts to CPR
4. Adjuncts for Airway Control and Ventilation
5. Management of Cardiac Arrest
6. Management of Symptomatic Bradycardia and Tachycardia


5. Management of Cardiac Arrest

5.1 Overview
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.

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.)

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.

The 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).

AHA Adult Advanced Cardiovascular Life Support
AHA Adult Advanced Cardiovascular Life Support

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.
* 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 per minute.
After placement of a supraglottic airway or an endotracheal tube, the provider performing chest compressions should deliver at least 100 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
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.

 

 

5.2 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.

5.2.1 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).

5.2.1.1 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.

5.2.1.1.1 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%)138 of biphasic shocks using 200 J or less for the first shock.138 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.

5.2.1.1.2 Recommendations
* 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)

5.2.1.2 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.

5.2.1.2.1 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. 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.

5.2.1.2.2 Recommendations
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)

5.2.1.3 Defibrillation Strategies for Ventricular Fibrillation or Pulseless Ventricular Tachycardia: Single Shocks Versus Stacked Shocks
5.2.1.3.2 Recommendation
* A single-shock strategy (as opposed to stacked shocks) is reasonable for defibrillation.


5.2.2 PEA/Asystole
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.

5.2.2.1 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. 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.

5.2.2.2 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)

 

 

5.3 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.

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.

5.3.2 Antiarrhythmic Drugs During and Immediately After Cardiac Arrest

5.3.2.1 Antiarrhythmic Therapy for Refractory VF/pVT Arrest
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.

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

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 polysorbate or 1.5 mg/kg lidocaine with polysorbate. 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. 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

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.

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, including VF/pVT. In these RCTs and in 1 additional randomized clinical trial, the use of magnesium in cardiac arrest for any rhythm presentation of cardiac arrest or strictly for VF arrest did not improve survival to hospital discharge or neurologic outcome.

5.3.2.1 Antiarrhythmic Drugs After Resuscitation


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 ß-adrenergic blocking drugs and lidocaine, and the evidence for their use is limited.

ß-adrenergicBlocking Drugs - Updated
ß-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. Conversely, ?-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 ?-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. 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. 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 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)
* There is inadequate evidence to support the routine use of a ?-blocker after cardiac arrest. However, the initiation or continuation of an oral or intravenous ?-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT. (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.

 

5.3.3 Vasopressors in Cardiac Arrest

Epinephrine and Vasopressin
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.

5.3.3.1 Standard-Dose Epinephrine - 2015 Updated
Epinephrine produces beneficial effects in patients during cardiac arrest, primarily because of its ß-adrenergic (ie, vasoconstrictor) effects.
These ß-adrenergic effects of epinephrine can increase coronary perfusion pressure and cerebral perfusion pressure during CPR.
The value and safety of the ß-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 Recommendation - Updated
* Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest.

5.3.3.2 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 ß-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), survival to discharge, or survival to hospital admission. There was, however, a demonstrated ROSC advantage with highdose epinephrine.

2015 Recommendation—New
* High-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III: No Benefit, LOE B-R)

5.3.3.3 Epinephrine Versus Vasopressin - Updated
Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction.

2015 Evidence Summary
A single RCT 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).

5.3.3.4 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, no benefit for survival to hospital discharge or hospital admission in 2438 patients, and no benefit for ROSC.

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)

5.3.3.5 Timing of Administration of Epinephrine - Updated
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.

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.

5.3.4 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.

5.3.4.1 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.
In a subsequent 3-center study published in 2013, 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.

5.3.4.2 2015 Evidence Summary: OHCA
In OHCA, steroids have been evaluated in 1 RCT and 1 observational study. 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.
The observational study 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 postarrest hydrocortisone as described by Mentzelopoulos et al 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)

5.7 Interventions Not Recommended for Routine Use During Cardiac Arrest

5.7.1 Atropine
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. 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)

5.7.2 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 increased ROSC, hospital admission, and survival to hospital discharge associated with use of bicarbonate. However, the majority of studies showed no benefit or found a relationship with poor outcome.

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. 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. 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. But clinical experience is greatly limited and outcome studies are lacking.

5.7.3 Calcium
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.

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

5.7.4 Fibrinolysis
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 and suggested benefit from fibrinolytic therapy in the treatment of victims of cardiopulmonary arrest unresponsive to standard therapy. But 2 large clinical trials 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.

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

5.7.5 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, and 2 animal studies showed that normothermic fluid infusion during CPR caused a decrease in CPP.
In addition to normothermic fluid, hypertonic and chilled fluids have been studied in animal and small human studies without a survival benefit.
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.

5.8 Pacing

Electric pacing is generally not effective in cardiac arrest, and no studies have observed a survival benefit from pacing in cardiac arrest. 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 (inhospital 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)

5.9 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.320 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. In 3 case series 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.

* 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.

5.10 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.

5.11 Summary

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

6.1 Overview
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 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 ß-adrenergic agonists with rateaccelerating 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

Intravenous Drugs Used to Treat Supraventricular Tachyarrhythmias

Drug: Adenosine
Characteristics: Endogenous purine nucleoside; briefly depresses sinus node rate and AV node conduction; vasodilator
Indication(s):
        * Stable, narrow-complex regular tachycardias
        * Unstable narrow-complex regular tachycardias while preparations are made for electrical cardioversion
        * Stable, regular, monomorphic, wide-complex tachycardia as a therapeutic and diagnostic maneuver
Dosing: 6 mg IV as a rapid IV push followed by a 20mL saline flush; repeat if required as 12 mg IV push
Side Effects: Hypotension, bronchospasm, chest discomfort
Precautions or Special Considerations: Contraindicated in patients with asthma; may precipitate atrial fibrillation, which may be very rapid in patients with WPW; thus a defibrillator should be readily available; reduce dose in post–cardiac transplant patients, those taking dipyridamole or carbamazepine and when administered via a central vein

Drug: Diltiazem, Verapamil
Characteristics: Non-dihydropyridine calcium channel blockers; slow AV node conduction and increase AV node refractoriness; vasodilators, negative inotropes
Indication(s):
        * Stable, narrow-complex tachycardias if rhythm remains uncontrolled or unconverted by adenosine or vagal maneuvers or if SVT is recurrent
        * Control ventricular rate in patients with atrial fibrillation or atrial flutter
Dosing:
* Diltiazem: Initial dose 15 to 20 mg (0.25 mg/kg) IV over 2 minutes; additional 20 to 25 mg (0.35 mg/kg) IV in 15 minutes if needed; 5 to 15 mg/h maintenance infusion (titrated to AF heart rate if given for rate control)
* 8Verapamil: Initial dose 2.5 to 5 mg IV given over 2 minutes; may repeat as 5 to 10 mg every 15 to 30 minutes to total dose of 20 to 30 mg
Side Effects: Hypotension, bradycardia, precipitation of heart failure
Precautions or Special Considerations: Should only be given to patients with narrow-complex tachycardias (regular or irregular). Avoid in patients with heart failure and pre-excited AF or flutter or rhythms consistent with VT

Drug: Atenolol, Esmolol, Metoprolol, Propranolol
Characteristics: ß-Blockers; reduce effects of circulating catecholamines; reduce heart rate, AV node conduction and blood pressure; negative inotropes
Indication(s):
* Stable, narrow-complex tachycardias if rhythm remains uncontrolled or unconverted by adenosine or vagal maneuvers or if SVT is recurrent
* Control ventricular rate in patients with atrial fibrillation or atrial flutter
* Certain forms of polymorphic VT (associated with acute ischemia, familial LQTS, catecholaminergic)
Dosing:
• Atenolol (ß1 specific blocker) 5 mg IV over 5 minutes; repeat 5 mg in 10 minutes if arrhythmia persists or recurs
• Esmolol (ß1 specific blocker with 2- to 9-minute half-life) IV loading dose 500 mcg/kg (0.5mg/kg) over 1 minute, followed by an infusion of 50 mcg/kg per minute (0.05mg/kg per minute); if response is inadequate, infuse second loading bolus of 0.5 mg/kg over 1 minute and increase maintenance infusion to 100 mcg/kg (0.1 mg/kg) per minute; increment: increase in this manner if required to maximum infusion rate of 300 mcg/kg [0.3 mg/kg] per minute
• Metoprolol (ß1 specific blocker) 5 mg over 1 to 2 minutes repeated as required every 5 minutes to maximum dose of 15 mg
• Propranolol (nonselective ß-blocker) 0.5 to 1 mg over 1 minute, repeated up to a total dose of 0.1 mg/kg if required
Side Effects: Hypotension, bradycardia, precipitation of heart failure
Precautions or Special Considerations: Avoid in patients with asthma, obstructive airway disease, decompensated heart failure and pre-excited artrial fibrillation or flutter

Drug: Procainamide
Characteristics: Sodium and potassium channel blocker
Indication(s): • Preexcited atrial fibrillation
Dosing: 20 to 50 mg/min until arrhythmia suppressed, hypotension ensues, or QRS prolonged by 50%, or total cumulative dose of 17 mg/kg; or 100 mg every 5 minutes until arrhythmia is controlled or other conditions described above are met
Side Effects: Bradycardia, hypotension, torsades de pointes
Precautions or Special Considerations: Avoid in patients with QT prolongation and CHF

Drug: Amiodarone
Characteristics: Multichannel blocker (sodium, potassium, calcium channel, and noncompetitive α/ß-blocker)
Indication(s):
        • Stable irregular narrow-complex tachycardia (atrial fibrillation)
        • Stable regular narrow-complex tachycardia
        • To control rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias
Dosing: 150 mg given over 10 minutes and repeated if necessary, followed by a 1 mg/min infusion for 6 hours, followed by 0.5 mg/min. Total dose over 24 hours should not exceed 2.2 g
Side Effects: Bradycardia, hypotension, phlebitis
Precautions or Special Considerations:

Drug: Digoxin
Characteristics: Cardiac glycoside with positive inotropic effects; slows AV node conduction by enhancing parasympathetic tone; slow onset of action
Indication(s):
        * Stable, narrow-complex regular tachycardias if rhythm remains uncontrolled or unconverted by adenosine or vagal maneuvers or if SVT is recurrent
        * Control ventricular rate in patients with atrial fibrillation or atrial flutter
Dosing: 8 to 12 mcg/kg total loading dose, half of which is administered initially over 5 minutes, and remaining portion as 25% fractions at 4- to 8-hour intervals
Side Effects: Bradycardia
Precautions or Special Considerations: Slow onset of action and relative low potency renders it less useful for treatment of acute arrhythmias

Intravenous Drugs Used to Treat Ventricular Tachyarrhythmias

Drug: Procainamide
Characteristics: Sodium and potassium channel blocker
Indication(s): • Hemodynamically stable monomorphic VT
Dosing: 20 to 50 mg/min until arrhythmia suppressed, hypotension ensues, or QRS prolonged by 50%, or total cumulative dose of 17 mg/kg; or 100 mg every 5 minutes until arrhythmia is controlled or other conditions described above are met
Side Effects: Bradycardia, hypotension, torsades de pointes
Precautions or Special Considerations: Avoid in patients with QT prolongation and CHF

Drug: Amiodarone
Characteristics: Multichannel blocker (sodium, potassium, calcium channel, α- and noncompetitive ß-blocker)
Indication(s):
        • Hemodynamically stable monomorphic VT
        • Polymorphic VT with normal QT interval
Dosing: 150 mg given over 10 minutes and repeated if necessary, followed by a 1 mg/min infusion for 6 hours, followed by 0.5 mg/min. Total dose over 24 hours should not exceed 2.2 g
Side Effects: Bradycardia, hypotension, phlebitis
Precautions or Special Considerations:

Drug: Sotalol
Characteristics: Potassium channel blocker and nonselective ß-blocker
Indication(s): • Hemodynamically stable monomorphic VT
Dosing: In clinical studies 1.5 mg/kg infused over 5 minutes; however, US package labeling recommends any dose of the drug should be infused slowly over a period of 5 hours
Side Effects: Bradycardia, hypotension, torsades de pointes
Precautions or Special Considerations: Avoid in patients with QT prolongation and CHF

Drug: Lidocaine
Characteristics: Relatively weak sodium channel blocker
Indication(s): • Hemodynamically stable monomorphic VT
Dosing: Initial dose range from 1 to 1.5 mg/kg IV; repeated if required at 0.5 to 0.75 mg/kg IV every 5 to 10 minutes up to maximum cumulative dose of 3 mg/kg; 1 to 4 mg/min (30 to 50 mcg/kg per minute) maintenance infusion
Side Effects: Slurred speech, altered consciousness, seizures, bradycardia
Precautions or Special Considerations:

Drug: Magnesium
Characteristics: Cofactor in variety of cell processes including control of sodium and potassium transport
Indication(s): • Polymorphic VT associated with QT prolongation (torsades de pointes)
Dosing: 1 to 2 g IV over 15 minutes
Side Effects: Hypotension, CNS toxicity, respiratory depression
Precautions or Special Considerations: Follow magnesium levels if frequent or prolonged dosing required, particularly in patients with impaired renal function

 

6.1.1 Bradycardia
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.


Adult Bradycardia With a Pulse Algorithm

6.1.1.1 Evaluation
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 (thirddegree) 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.

Adult Bradycardia With a Pulse Algorithm

6.1.1.2 Therapy (Figure 3 Box 5)

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

Clinical trials in adults 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.

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. 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.

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 ß-adrenergic support as temporizing measures while the patient is prepared for transvenous pacing (Figure 3, Box 6).

2 Pacing
* It is reasonable for healthcare providers to initiate transcutaneous pacing (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)

3 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 ß-blocker or calcium channel blocker.

3.1 Dopamine
Dopamine hydrochloride is a catecholamine with both α- and ß-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. Use of vasoconstrictors requires that the recipient be assessed for adequate intravascular volume and volume status supported as needed.

3.2 Epinephrine
Epinephrine is a catecholamine with α- and ß-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.

3.3 Isoproterenol
Isoproterenol is a ß-adrenergic agent with ß-1 and ß-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.

 

6.2 Tachycardia
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.


Adult Tachycardia With a Pulse Algorithm

6.2.1 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, narrowcomplex 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 widecomplex (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.

6.2.2 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.

6.2.3 Cardioversion
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. 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. (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 sufficient. If the initial 50-J shock fails, the provider should increase the dose in a stepwise fashion.

* Cardioversion of atrial fabrillation with monophasic waveforms should begin at 200 J and increase in stepwise fashion if not successful. (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 highenergy unsynchronized shocks (ie, defibrillation doses). Use the ACLS Cardiac Arrest Algorithms in this document above under 4.1: “Management of Cardiac Arrest.”

 

Supravetricular tachycardia (SVT)

Due to increased automaticity or re-entry.
4 main types:
1. Atrial fibrillation
2. Atrial flutter
3. Paroxysmal Supravetricular tachycardia (PSVT)
4. Wolff-Parkinson-White syndrome (WPW).

Atrial origin:
Sinoatrial node reentrant tachycardia (SANRT) is caused by reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size before a regular, narrow QRS complex. It cannot be EKG distinguished from sinus tachycardia unless sudden onset is observed. It may sometimes be distinguished by its prompt response to vagal maneuvers.

Atrial tachycardia (ectopic unifocal atrial tachycardia) can exhibit consistent heart rates from 140 to 220 beats per minute.
It is a risk factor for atrial fibrillation.

Multifocal atrial tachycardia (or Multifocal atrial rhythm if the heart rate is ≦100)
Common in older patients and is associated with exacerbation of COPD.
EKG diagnosis: Regular atrial rhythm (tachycardia) with variable P wave shapes.

Atrial fibrillation:
Irregular impulses reaching AV node, only some being transmitted.
EKG characterized by irregulat and rapid atrial rhythm with variable P wave shapes and irregular ventricular responses

Atrial flutter is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute.
On the EKG this appears as a line of "sawtooth" waves preceding the QRS complex.
The AV node will not usually conduct 300 beats per minute so the P:QRS ratio is usually 2:1 or 4:1 pattern. (Rarely 3:1 and sometimes 1:1 when IC antiarrhythmic drugs are in use.)

AV node origin:
AV node reentrant tachycardia (AVNRT)
Involves a reentry circuit forming next to, or within, the AV node.
Because the node is located between the atria and ventricle, the re-entry circuit often stimulates both atria and ventricle, appearing as a backkward conducted P-wave buried within of occuring just afterthe regular, narrow QRS complexes.

AV reciprocating tachycardia (AVRT):
Also results from a reentry circuit. One portion of the circuit is usually Av node, and the other, an abnormal accessary pathway.

Junctional ectopic tachycardia (JET):
A rare tachycardia caused by increased automaticity of the AV node itself. It is often due to drug toxicity.
EKG findings: Abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complexes.

Accessory pathway bypassing AV node:
Wolff-Parkinson-White syndrome (Ventricular pre-excitation with arrhythmia):
Individuals have an accessory pathway (the bundle of Kent) that communicates between the atria and the ventricles.
EKG Diagnosis: Short PR interval, characteristic "delta wave" and wide QRS complex.

Paroxysmal supravetricular tachycardia (PSVT)

AV nadal re-entrant tachycardia (AVNRT) 56%
AV reciprocating tachycardia (AVRT) 27%
Paroxysmal atrial tachycardia 17%

 

6.2.4 Regular Narrow-Complex Tachycardia

1. 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.

2. Supraventricular Tachycardia (Reentry SVT)
Evaluation
The rhythm (tachycardia) 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.

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.
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.

Therapy for Regular Narrow-Complex Tachycardia
1. 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. 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.

2. Adenosine
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 studies support the use of adenosine in the treatment of stable PSVT. Although 2 randomized clinical trials 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, and the potential proarrhythmic risks of these agents favor the use of safer treatment alternatives.

Adenosine is safe and effective in pregnancy. 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. 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 ß-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.

3. Calcium Channel Blockers and ß-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 ß-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 verapamil, and diltiazem, 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 ß-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 ß-blockers can include bradycardias, AV conduction delays, and hypotension. ß-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, ß-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 ß-blocker. Conversely the longer half-life of a calcium channel or ß-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.

6.2.5 Wide-Complex Tachycardia

Evaluation
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 widecomplex 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. (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 studies showed that adenosine converted an undifferentiated wide-complex tachycardia to sinus rhythm. Another study 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,384 conversion to VF in 4 patients with pre-excited atrial fibrillation, conversion to VF in 2 patients with WPW,386 and a single case of VF in a patient with VT.

* 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. Profound hypotension was reported in 11 of 25 patients known to have VT treated with verapamil.

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. 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.

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. 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 arrhythmias, 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 reports, 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, and when given to patients with or without a history of MI with spontaneous sustained stable VT in the hospital setting. Lidocaine has been reported to variably terminate VT when administered intramuscularly to patients with AMI and VT in the out-of-hospital setting. 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).

 

6.3 Irregular Tachycardias

6.3.1 Atrial Fibrillation and Flutter
Evaluation
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.

Therapy
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.

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

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

A wide-complex 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 ß-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.

6.3.2 Polymorphic (Irregular) VT
Polymorphic (irregular) VT requires immediate defibrillation with the same strategy used for VF. Pharmacologic treatment to prevent recurrent polymorphic VT should be directed by the underlying cause of VT and the presence or absence of a long QT interval during sinus rhythm.

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 studies that showed effectiveness in patients with prolonged QT interval. One adult case series 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 ß-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 ß-blockers may reduce the frequency of arrhythmia recurrence. (Class IIb, LOE C)

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

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

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

6.4 Summary
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.

 

 

 

5.4 Access for Parenteral Medications During Cardiac Arrest

5.4.1 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 studies 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 study the interval from first shock to administration of an antiarrhythmic drug was a significant predictor of survival. One animal study 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. 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.

5.4.2 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. 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.

5.4.3 IO Drug Delivery (Intraosseous)
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 children and adults and 6 other studies 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.)

5.4.4 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. 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. 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.

5.4.5 Endotracheal Drug Delivery
* If IV or IO access cannot be established, epinephrine, vasopressin, and lidocaine may be administered by the endotracheal route during cardiac arrest. (Class IIb, LOE B)

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. 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. Studies with epinephrine and lidocaine showed that dilution with sterile water instead of 0.9% saline may achieve better drug absorption.

 

3. Adjuncts to CPR - Updated

Oxygen Dose During CPR: When supplementary oxygen is available, it may be reasonable to use the maximal feasible inspired oxygen concentration during CPR.

3.3 Monitoring Physiologic Parameters During CPR - Updated
Monitoring both provider performance and patient physiologic parameters during CPR is essential to optimizing CPR quality.

3.3.1 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. These parameters can be monitored continuously, without interrupting chest compressions. An abrupt increase in any of these parameters is a sensitive indicator of ROSC. There is evidence that these and other physiologic parameters can be modified by interventions aimed at improving CPR quality.

3.3.2 Recommendation
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)

Ultrasound (cardiac or noncardiac) may be considered during the management of cardiac arrest, although its usefulness has not been well established.
(If a qualified sonographer is present and use of ultrasound does not interfere with the standard
arrest treatment protocol, then ultrasound may be considered as an adjunct to standard patient evaluation.)

4 Adjuncts for Airway Control and Ventilation

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. 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 positivepressure 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.

* 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. 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 bagmask 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 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.

* Bag-Mask Ventilation Compared With Any Advanced Airway During CPR
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 bagmask 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.
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 intubation or other advanced airway devices. 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 studies showed no difference in survival.

Advanced Airways
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.

* 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.

* 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.

* For healthcare providers trained in their use, either an SGA device or an ETT may be used as the initial advanced airway during CPR.

* 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.

 

 

 

Cardiopulmonary Resuscitation (CPR)
in Infants and Children (Merck Manual)


Cardiopulmonary Resuscitation (CPR) in Adults (Merck Manual)

By Robert E O’Connor, MD, MPH, Professor and Chair of Emergency Medicine, University of Virginia School of Medicine

 

CPR is an organized, sequential response to cardiac arrest, including
  • Recognition of absent breathing and circulation
  • Basic life support with chest compressions and rescue breathing
  • Advanced cardiac life support (ACLS) with definitive airway and rhythm control
  • Postresuscitative care

Prompt initiation of uninterrupted chest compression and early defibrillation (when indicated) are the keys to success. Speed, efficiency, and proper application of CPR with the least possible interruptions determine successful outcome; the rare exception is profound hypothermia caused by cold water immersion, when successful resuscitation may be accomplished even after prolonged arrest (up to 60 min).

CONTENT:
        Overview of CPR
        Airway and Breathing
        Circulation
        Defibrillation
        Monitor and IV
        Special Circumstances
        Drugs for ACLS
        Dysrhythmia Treatment
        Termination of Resuscitation
        Postresuscitative Care
        More Information

Overview of CPR
Guidelines for health care professionals from the American Heart Association are followed (see Figure: Adult comprehensive emergency cardiac care.). If a person has collapsed with possible cardiac arrest, a rescuer first establishes unresponsiveness and confirms absence of breathing or the presence of only gasping respirations. Then, the rescuer calls for help. Anyone answering is directed to activate the emergency response system (or appropriate in-hospital resuscitation personnel) and, if possible, obtain a defibrillator.

If no one responds, the rescuer first activates the emergency response system and then begins basic life support by giving 30 chest compressions at a rate of 100 to 120/min and then opening the airway (lifting the chin and tilting back the forehead) and giving 2 rescue breaths. The cycle of compressions and breaths is continued (see Table: CPR Techniques for Health Care Practitioners) without interruption; preferably each rescuer is relieved every 2 min.

When a defibrillator (manual or automated) becomes available, a person in ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) is given an unsynchronized shock (see also Defibrillation). If the cardiac arrest is witnessed and a defibrillator is on the scene, a person in VF or VT is immediately defibrillated; early defibrillation may promptly convert VF or pulseless VT to a perfusing rhythm. It is recommended that untrained bystanders begin and maintain continuous chest compressions until skilled help arrives.

 

Adult comprehensive emergency cardiac care

Adult comprehensive emergency cardiac care.
if an adequate number of trained personnel are available, patient assessment, CPR, and activation of the emergency response system should occur simultaneously.


Adult comprehensive emergency cardiac care

Airway and Breathing
Opening the airway is given 2nd priority (see Clearing and Opening the Upper Airway) after beginning chest compressions. For mechanical measures regarding resuscitation in children, see Table: Guide to Pediatric Resuscitation—Mechanical Measures.

Mouth-to-mouth (adults, adolescents, and children) or combined mouth-to-mouth-and-nose (infants) rescue breathing or bag-valve-mask ventilation is begun for asphyxial cardiac arrest. If available, an oropharyngeal airway may be inserted. Cricoid pressure is no longer recommended.

If abdominal distention develops, the airway is rechecked for patency and the amount of air delivered during rescue breathing is reduced. Nasogastric intubation to relieve gastric distention is delayed until suction equipment is available because regurgitation with aspiration of gastric contents may occur during insertion. If marked gastric distention interferes with ventilation and cannot be corrected by the above methods, patients are positioned on their side, the epigastrium is compressed, and the airway is cleared.

When qualified providers are present, an advanced airway (endotracheal tube or supraglottic device) is placed without interruption of chest compression as described under Airway Establishment and Control. A breath is given every 6 sec (10 breaths/min) without interrupting chest compression. However, chest compression and defibrillation take precedence over endotracheal intubation. Unless highly experienced providers are available, endotracheal intubation may be delayed in favor of ventilation with bag-valve-mask, laryngeal mask airway, or similar device.

Circulation
        Chest compression
In witnessed cardiac arrest, chest compression should be done until defibrillation is available. In an unresponsive patient whose collapse was unwitnessed, the trained rescuer should immediately begin external (closed chest) cardiac compression, followed by rescue breathing. Chest compressions must not be interrupted for >10 sec (eg, for intubation, central IV catheter placement, or transport). A compression cycle should consist of 50% compression and 50% release; during the release phase, it is important to allow the chest to recoil fully. Rhythm interpretation and defibrillation (if appropriate) are done as soon as a defibrillator is available.

The recommended chest compression depth for adults is between 2 and 2.4 in (about 5 to 6 cm). Ideally, external cardiac compression produces a palpable pulse with each compression, although cardiac output is only 20 to 30% of normal. However, palpation of pulses during chest compression is difficult, even for experienced clinicians, and often unreliable. End-tidal carbon dioxide monitoring provides a better estimate of cardiac output during chest compression; patients with inadequate perfusion have little venous return to the lungs and hence a low end-tidal carbon dioxide. Restoration of spontaneous breathing or eye opening indicates restoration of spontaneous circulation.

Mechanical chest compression devices are available; these devices are no more effective than properly executed manual compressions but can minimize effects of performance error and fatigue and can be helpful in some circumstances, such as during patient transport or in the cardiac catheterization laboratory.

Open-chest cardiac compression may be effective but is used only in patients with penetrating chest injuries, shortly after cardiac surgery (ie, within 48 h), in cases of cardiac tamponade, and most especially after cardiac arrest in the operating room when the patient’s chest is already open. However, thoracotomy requires training and experience and is best done only within these limited indications.

        Complications of chest compression
Laceration of the liver is a rare but potentially serious (sometimes fatal) complication and is usually caused by compressing the abdomen below the sternum. Rupture of the stomach (particularly if the stomach is distended with air) is also a rare complication. Delayed rupture of the spleen is very rare. An occasional complication, however, is regurgitation followed by aspiration of gastric contents, causing life-threatening aspiration pneumonia in resuscitated patients.

Costochondral separation and fractured ribs often cannot be avoided because it is important to compress the chest deeply enough to produce sufficient blood flow. Fractures are quite rare in children because of the flexibility of the chest wall. Bone marrow emboli to the lungs have rarely been reported after external cardiac compression, but there is no clear evidence that they contribute to mortality. Lung injury is rare, but pneumothorax after a penetrating rib fracture may occur. Serious myocardial injury caused by compression is very unlikely, with the possible exception of injury to a preexisting ventricular aneurysm. Concern for these injuries should not deter the rescuer from doing CPR.

 

Defibrillation
The most common rhythm in witnessed adult cardiac arrest is ventricular fibrillation (VF); rapid conversion to a perfusing rhythm is essential. Pulseless ventricular tachycardia (VT) is treated the same as VF.

Prompt direct-current cardioversion is more effective than antiarrhythmic drugs; however, the success of defibrillation is time dependent, with about a 10% decline in success after each minute of VF (or pulseless VT). Automated external defibrillators (AEDs) allow minimally trained rescuers to treat VT or VF. Their use by first responders (police and fire services) and their prominent availability in public locations has increased the likelihood of resuscitation.

Defibrillating paddles or pads are placed between the clavicle and the 2nd intercostal space along the right sternal border and over the 5th or 6th intercostal space at the apex of the heart (in the mid-axillary line). Conventional defibrillator paddles are used with conducting paste; pads have conductive gel incorporated into them. Only 1 initial countershock is now advised (the previous recommendation was 3 stacked shocks), after which chest compression is resumed. Energy level for biphasic defibrillators is between 120 and 200 joules (2 joules/kg in children) for the initial shock; monophasic defibrillators are set at 360 joules for the initial shock. Postshock rhythm is not checked until after 2 min of chest compression. Subsequent shocks are delivered at the same or higher energy level (maximum 360 joules in adults, or 10 joules/kg in children). Patients remaining in VF or VT receive continued chest compression and ventilation and optional drug therapy.

Monitor and IV
ECG monitoring is established to identify the underlying cardiac rhythm. An IV line may be started; 2 lines minimize the risk of losing IV access during CPR. Large-bore peripheral lines in the antecubital veins are preferred. In adults and children, if a peripheral line cannot be established, a subclavian or internal jugular central line (see Procedure) can be placed provided it can be done without stopping chest compression (often difficult). Intraosseous and femoral lines (see Intraosseous Infusion) are the preferred alternatives, especially in children. Femoral vein catheters (see Procedure), preferably long catheters advanced centrally, are an option because CPR does not need to be stopped and they have less potential for lethal complications; however, they may have a lower rate of successful placement because no discrete femoral arterial pulsations are available to guide insertion.

The type and volume of fluids or drugs given depend on the clinical circumstances. Usually, IV 0.9% saline is given slowly (sufficient only to keep an IV line open); vigorous volume replacement (crystalloid and colloid solutions, blood) is required only when arrest results from hypovolemia (see Intravenous Fluid Resuscitation).

Special Circumstances
In accidental electrical shock, rescuers must be certain that the patient is no longer in contact with the electrical source to avoid shocking themselves. Use of nonmetallic grapples or rods and grounding of the rescuer allows for safe removal of the patient before starting CPR.

In near drowning, rescue breathing may be started in shallow water, although chest compression is not likely to be effectively done until the patient is placed horizontally on a firm surface, such as a surfboard or float.

If cardiac arrest follows traumatic injury, airway opening maneuvers and a brief period of external ventilation after clearing the airway have the highest priority because airway obstruction is the most likely treatable cause of arrest. To minimize cervical spine injury, jaw thrust, but not head tilt and chin lift, is advised. Other survivable causes of traumatic cardiac arrest include cardiac tamponade and tension pneumothorax, for which immediate needle decompression is lifesaving. However, most patients with traumatic cardiac arrest have severe hypovolemia due to blood loss (for which chest compression may be ineffective) or nonsurvivable brain injuries.

 

Drugs for ACLS (Advanced cardiac life support)
Despite widespread and long-standing use, no drug or drug combination has been definitively shown to increase survival to hospital discharge in patients with cardiac arrest. Some drugs do seem to improve the likelihood of restoration of spontaneous circulation (ROSC) and thus may reasonably be given (for dosing, including pediatric, see Table: Drugs for Resuscitation*). Drug therapy for shock and cardiac arrest continues to be researched.

In a patient with a peripheral IV line, drug administration is followed by a fluid bolus (“wide open” IV in adults; 3 to 5 mL in young children) to flush the drug into the central circulation. In a patient without IV or intraosseous access, naloxone, atropine, and epinephrine, when indicated, may be given via the endotracheal tube at 2 to 2.5 times the IV dose. During administration of a drug via endotracheal tube, compression should be briefly stopped.

        First-line drugs
The main first-line drug used in cardiac arrest is
• Epinephrine
Epinephrine may be given 1 mg IV q 3 to 5 min. It has combined adrenergic and beta-adrenergic effects.
The alpha-adrenergic effects may augment coronary diastolic pressure, thereby increasing subendocardial perfusion during chest compressions. Epinephrine also increases the likelihood of successful defibrillation. However, beta-adrenergic effects may be detrimental because they increase oxygen requirements (especially of the heart) and cause vasodilation. Intracardiac injection of epinephrine is not recommended because, in addition to interrupting precordial compression, pneumothorax, coronary laceration, and cardiac tamponade may occur.

Amiodarone 300 mg can be given once if defibrillation is unsuccessful after epinephrine, followed by 1 dose of 150 mg. It is also of potential value if VT or VF recurs after successful defibrillation; a lower dose is given over 10 min followed by a continuous infusion. There is no persuasive proof that it increases survival to hospital discharge.

A single dose of vasopressin 40 units, which has a duration of activity of 40 min, is an alternative to epinephrine (adults only). However, it is no more effective than epinephrine and is therefore no longer recommended in the American Heart Association's guidelines. However, in the unlikely case of a lack of epinephrine during CPR, vasopressin may be substituted.

        Other drugs
A range of additional drugs may be useful in specific settings.
Atropine sulfate is a vagolytic drug that increases heart rate and conduction through the atrioventricular node. It is given for symptomatic bradyarrhythmias and high-degree atrioventricular nodal block. It is no longer recommended for asystole or pulseless electrical activity.

Calcium chloride is recommended for patients with hyperkalemia, hypermagnesemia, hypocalcemia, or calcium channel blocker toxicity. In other patients, because intracellular calcium is already higher than normal, additional calcium is likely to be detrimental. Because cardiac arrest in patients on renal dialysis is often a result of or accompanied by hyperkalemia, these patients may benefit from a trial of calcium if bedside potassium determination is unavailable. Caution is necessary because calcium exacerbates digitalis toxicity and can cause cardiac arrest.

Magnesium sulfate has not been shown to improve outcome in randomized clinical studies. However, it may be helpful in patients with torsades de pointes or known or suspected magnesium deficiency (ie, alcoholics, patients with protracted diarrhea).

Procainamide is a 2nd-line drug for treatment of refractory VF or VT. However, procainamide is not recommended for pulseless arrest in children.

Phenytoin may rarely be used to treat VF or VT, but only when VF or VT is due to digitalis toxicity and is refractory to other drugs. A dose of 50 to 100 mg/min q 5 min is given until rhythm improves or the total dose reaches 20 mg/kg.

Sodium bicarbonate is no longer recommended unless cardiac arrest is caused by hyperkalemia, hypermagnesemia, or tricyclic antidepressant overdose with complex ventricular arrhythmias. In children, sodium bicarbonate may be considered when cardiac arrest is prolonged (> 10 min); it is given only if there is good ventilation. When sodium bicarbonate is used, arterial pH should be monitored before infusion and after each 50-mEq dose (1 to 2 mEq/kg in children).

Lidocaine is not recommended for routine use during cardiac arrest. However, it may be helpful as an alternative to amiodarone for VF or VT that is unresponsive to defibrillation (in children) or after ROSC (Return of Spontaneous Circulation) due to VF or VT (in adults).

Bretylium is no longer recommended for management of cardiac arrest.

 

 

Dysrhythmia Treatment
VF or pulseless VT is treated with one direct-current shock, preferably with biphasic waveform, as soon as possible after those rhythms are identified. Despite some laboratory evidence to the contrary, it is not recommended to delay defibrillation to administer a period of chest compressions. Chest compression should be interrupted as little as possible and for no more than 10 sec at a time for defibrillation. Recommended energy levels for defibrillation vary: 120 to 200 joules for biphasic waveform and 360 joules for monophasic. If this treatment is unsuccessful, epinephrine 1 mg IV is administered and repeated q 3 to 5 min. Defibrillation at the same energy level or higher is attempted 1 min after each drug administration. If VF persists, amiodarone 300 mg IV is given. Then, if VF/VT recurs, 150 mg is given followed by infusion of 1 mg/min for 6 h, then 0.5 mg/min. Current versions of AEDs provide a pediatric cable that effectively reduces the energy delivered to children. (For pediatric energy levels, see Defibrillation; for drug doses, see Table: Drugs for Resuscitation*.)

Asystole can be mimicked by a loose or disconnected monitor lead; thus, monitor connections should be checked and the rhythm viewed in an alternative lead. If asystole is confirmed, the patient is given epinephrine 1 mg IV repeated q 3 to 5 min. Defibrillation of apparent asystole (because it “might be fine VF”) is discouraged because electrical shocks injure the nonperfused heart.

Pulseless electrical activity is circulatory collapse that occurs despite satisfactory electrical complexes on the ECG. Patients with pulseless electrical activity receive 500- to 1000-mL (20 mL/kg) infusion of 0.9% saline. Epinephrine may be given in amounts of 0.5 to 1.0 mg IV repeated q 3 to 5 min. Cardiac tamponade can cause pulseless electrical activity, but this disorder usually occurs in patients after thoracotomy and in patients with known pericardial effusion or major chest trauma. In such settings, immediate pericardiocentesis or thoracotomy is done (see Figure: Pericardiocentesis.). Tamponade is rarely an occult cause of cardiac arrest but, if suspected, can be confirmed by ultrasonography or, if ultrasonography is unavailable, pericardiocentesis.

Termination of Resuscitation
CPR should be continued until the cardiopulmonary system is stabilized, the patient is pronounced dead, or a lone rescuer is physically unable to continue. If cardiac arrest is thought to be due to hypothermia, CPR should be continued until the body is rewarmed to 34° C.

The decision to terminate resuscitation is a clinical one, and clinicians take into account duration of arrest, age of the patient, and prognosis of underlying medical conditions. The decision is typically made when spontaneous circulation has not been established after CPR and ACLS measures have been done. In intubated patients, an end-tidal carbon dioxide (ETCO2) level of < 10 mm Hg is a poor prognostic sign.

 

Postresuscitative Care
Restoration of spontaneous circulation (ROSC) is only an intermediate goal in resuscitation. The ultimate goal is survival to hospital discharge with good neurologic function, which is achieved by only a minority of patients with ROSC. To maximize the likelihood of a good outcome, clinicians must provide good supportive care (eg, manage blood pressure, temperature, and cardiac rhythm) and treat underlying conditions, particularly acute coronary syndromes.

Postresuscitation laboratory studies include ABG, CBC, and blood chemistries, including electrolytes, glucose, BUN, creatinine, and cardiac markers. (Creatine kinase is usually elevated because of skeletal muscle damage caused by CPR; troponins, which are unlikely to be affected by CPR or defibrillation, are preferred.) Arterial Pao2 should be kept near normal values (80 to 100 mm Hg). Hct should be maintained at ≥ 30 (if cardiac etiology is suspected), and glucose at 140 to 180 mg/dL; electrolytes, especially potassium, should be within the normal range.

        Coronary angiography
When indicated, coronary angiography should be done emergently (rather than later during the hospital course) so that if percutaneous coronary intervention (PCI) is needed, it is done as soon as possible. The decision to do cardiac catheterization after resuscitation from cardiac arrest should be individualized based on the ECG, the interventional cardiologist's clinical impression, and the patient's prognosis. However, guidelines suggest doing emergency angiography for adult patients in whom a cardiac cause is suspected and who have
• ST-segment elevation on the ECG
• Coma with no ST-segment elevation


        Neurologic support
Only about 10% of all cardiac arrest survivors have good CNS function (cerebral performance index 1 or 2) at hospital discharge. Hypoxic brain injury is a result of ischemic damage and cerebral edema (see pathophysiology of cardiac arrest). Both damage and recovery may evolve over 48 to 72 h after resuscitation.

Maintenance of oxygenation and cerebral perfusion pressure (avoiding hypotension) may reduce cerebral complications. Both hypoglycemia and hyperglycemia may damage the post-ischemic brain and should be treated.

In adults, targeted temperature management (maintaining body temperature of 32 to 36° C) is recommended for patients who remain unresponsive after spontaneous circulation has returned (1, 2). Cooling is begun as soon as spontaneous circulation has returned. Techniques to induce and maintain hypothermia can be either external or invasive. External cooling methods are easy to apply and range from the use of external ice packs to several commercially available external cooling devices that circulate high volumes of chilled water over the skin. For internal cooling, chilled IV fluids (4° C) can be rapidly infused to lower body temperature, but this method may be problematic in patients who cannot tolerate much additional fluid volume. Also available are external heat-exchange devices that circulate chilled saline to an indwelling IV heat-exchange catheter using a closed-loop design in which chilled saline circulates through the catheter and back to the device, rather than into the patient. Another invasive method for cooling uses an extracorporeal device that circulates and cools blood externally then returns it to the central circulation. Regardless of the method chosen, the goal is to cool the patient rapidly and to maintain the core temperature between 32° C and 36° C. Currently, there is no evidence that any specific temperature within this range is superior, but it is imperative to avoid hyperthermia.

Numerous pharmacologic treatments, including free radical scavengers, antioxidants, glutamate inhibitors, and calcium channel blockers, are of theoretic benefit; many have been successful in animal models, but none have proved effective in human trials.

        Blood pressure support
Current recommendations are to maintain a mean arterial pressure (MAP) of > 80 mm Hg in older adults or > 60 mm Hg in younger and previously healthy patients. In patients known to be hypertensive, a reasonable target is systolic BP 30 mm Hg below prearrest level. MAP is best measured with an intra-arterial catheter. Use of a flow-directed pulmonary artery catheter for hemodynamic monitoring has been largely discarded.

BP support includes
• IV 0.9% saline
• Sometimes inotropic or vasopressor drugs
• Rarely intra-aortic balloon counterpulsation

Patients with low MAP and low central venous pressure should have IV fluid challenge with 0.9% saline infused in 250-mL increments.

Clinical Calculator: Mean Vascular Pressure (systemic or pulmonary)

Although use of inotropic and vasopressor drugs has not proved to enhance long-term survival, older adults with moderately low MAP (70 to 80 mm Hg) and normal or high central venous pressure may receive an infusion of an inotrope (eg, dobutamine started at 2 to 5 mcg/kg/min). Alternatively, amrinone or milrinone is used (see Table: Drugs for Resuscitation*).

If this therapy is ineffective, the inotrope and vasoconstrictor dopamine may be considered. Alternatives are epinephrine and the peripheral vasoconstrictors norepinephrine and phenylephrine (see Table: Drugs for Resuscitation*). However, vasoactive drugs should be used at the minimal dose necessary to achieve low-normal MAP because they may increase vascular resistance and decrease organ perfusion, especially in the mesenteric bed. They also increase the workload of the heart at a time when its capability is decreased because of postresuscitation myocardial dysfunction.

If MAP remains < 70 mm Hg in patients who may have sustained an MI, intra-aortic balloon counterpulsation should be considered. Patients with normal MAP and high central venous pressure may improve with either inotropic therapy or afterload reduction with nitroprusside or nitroglycerin.

Intra-aortic balloon counterpulsation can assist low-output circulatory states due to left ventricular pump failure that is refractory to drugs. A balloon catheter is introduced via the femoral artery, percutaneously or by arteriotomy, retrograde into the thoracic aorta just distal to the left subclavian artery. The balloon inflates during each diastole, augmenting coronary artery perfusion, and deflates during systole, decreasing afterload. Its primary value is as a temporizing measure when the cause of shock is potentially correctable by surgery or percutaneous intervention (eg, acute MI with major coronary obstruction, acute mitral insufficiency, ventricular septal defect).

        Dysrhythmia treatment
Although VF or VT may recur after resuscitation, prophylactic antiarrhythmic drugs do not improve survival and are no longer routinely used. However, patients manifesting such rhythms may be treated with procainamide (see Other drugs) or amiodarone (see First-line drugs).

Postresuscitation rapid supraventricular tachycardias occur frequently because of high levels of beta-adrenergic catecholamines (both endogenous and exogenous) during cardiac arrest and resuscitation. These rhythms should be treated if extreme, prolonged, or associated with hypotension or signs of coronary ischemia. An esmolol IV infusion is given, beginning at 50 mcg/kg/min.

Patients who had arrest caused by VF or VT not associated with acute MI are candidates for an implantable cardioverter-defibrillator (ICD). Current ICDs are implanted similarly to pacemakers and have intracardiac leads and sometimes subcutaneous electrodes. They can sense arrhythmias and deliver either cardioversion or cardiac pacing as indicated.

 

 

Summary

CPR is an organized, sequential response to cardiac arrest, including
• Recognition of absent breathing and circulation
• Basic life support with chest compressions and rescue breathing
• Advanced cardiac life support (ACLS) with definitive airway and rhythm control
• Postresuscitative care


* Person collapse and unresponsive. Possible cardiac arrest.
* Call (or ask a bystander to call) 911, then send someone to get an AED (Automated External Defibrillator) if available.
* Check to see if there is a pulse and breathing. If there is no breathing or a pulse within 10 seconds, begin CPR.
* If the person is not breathing but has a pulse, give rescue breaths 10-12 breaths/min (one breath every 5-6 seconds).
(Open the airway by lifting the chin and tilting back the forehead. Each breath about 500 ml, caution against hyperventilation.)
* If there is no breathing and no pulse, start CPR with 30 chest compressions (at a rate of 100 to 120/min) followed by two rescue breaths (1 second each).
* The cycle of compressions and breaths is continued without interruption, preferably each rescuer is relieved every 2 min.

* If a defibrillator is on the scene, a person in VF or pulseless VT (pVT) is immediately defibrillated.
* It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm (asystole or PEA).
(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.)
*Airway and Breathing: Opening the airway is given 2nd priority after beginning chest compressions.
Mouth-to-mouth (adults, adolescents, and children) or combined mouth-to-mouth-and-nose (infants) rescue breathing or bag-valve-mask ventilation is begun for asphyxial cardiac arrest. If available, an oropharyngeal airway may be inserted. Cricoid pressure is no longer recommended.

■ 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.
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.
Fibrinolytic therapy administered during CPR for acute coronary occlusion has not been shown to improve outcome.


First-line drugs, Defibrillation and Advanced airway
* Epinephrine 1 mg IV every 3 to 5 min.
(Intracardiac injection of epinephrine is not recommended because, in addition to interrupting precordial compression, pneumothorax, coronary laceration, and cardiac tamponade may occur.)
* Repeat defibrillation if needed.
* When qualified providers are present, an advanced airway (endotracheal tube or supraglottic device) is placed without interruption of chest compression. A breath is given every 6 sec (10 breaths/min) without interrupting chest compression. However, chest compression and defibrillation take precedence over endotracheal intubation. Unless highly experienced providers are available, endotracheal intubation may be delayed in favor of ventilation with bag-valve-mask, laryngeal mask airway, or similar device.

If defibrillation is unsuccessful after epinephrine
* Amiodarone 300 mg (IV push over 2 min) can be given once if defibrillation is unsuccessful after epinephrine, followed by 1 dose of 150 mg.
It is also of potential value if VT or VF recurs after successful defibrillation; a lower dose (150 mg) is given over 10 min followed by a continuous infusion (1 mg/min × 6 h, then 0.5 mg/min × 24 h). There is no persuasive proof that it increases survival to hospital discharge.
* A single dose of vasopressin 40 units, which has a duration of activity of 40 min, is an alternative to epinephrine (adults only).
However, it is no more effective than epinephrine and is therefore no longer recommended in the American Heart Association's guidelines.
However, in the unlikely case of a lack of epinephrine during CPR, vasopressin may be substituted.
        (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.)
Other drugs:
* Procainamide is a 2nd-line drug for treatment of refractory VF or VT. However, procainamide is not recommended for pulseless arrest in children.
* Lidocaine is not recommended for routine use during cardiac arrest. However, it may be helpful as an alternative to amiodarone for VF or VT that is unresponsive to defibrillation (in children) or after ROSC (Return of Spontaneous Circulation) due to VF or VT (in adults).
* Phenytoin may rarely be used to treat VF or VT, but only when VF or VT is due to digitalis toxicity and is refractory to other drugs. A dose of 50 to 100 mg/min q 5 min is given until rhythm improves or the total dose reaches 20 mg/kg.
* Atropine sulfate is a vagolytic drug that increases heart rate and conduction through the atrioventricular node. It is given for symptomatic bradyarrhythmias and high-degree atrioventricular nodal block. It is no longer recommended for asystole or pulseless electrical activity.
* Calcium chloride is recommended for patients with hyperkalemia, hypermagnesemia, hypocalcemia, or calcium channel blocker toxicity.
In other patients, because intracellular calcium is already higher than normal, additional calcium is likely to be detrimental.
Because cardiac arrest in patients on renal dialysis is often a result of or accompanied by hyperkalemia, these patients may benefit from a trial of calcium if bedside potassium determination is unavailable. Caution is necessary because calcium exacerbates digitalis toxicity and can cause cardiac arrest.
* The routine use of magnesium for VF/pVT is not recommended in adult patients. (Class III: No Benefit, LOE B-R)
Magnesium sulfate has not been shown to improve outcome in randomized clinical studies.
(However, it may be helpful in patients with torsades de pointes or known or suspected magnesium deficiency, ie, alcoholics, patients with protracted diarrhea.).
* Sodium bicarbonate is no longer recommended unless cardiac arrest is caused by hyperkalemia, hypermagnesemia, or tricyclic antidepressant overdose with complex ventricular arrhythmias. In children, sodium bicarbonate may be considered when cardiac arrest is prolonged (> 10 min); it is given only if there is good ventilation. When sodium bicarbonate is used, arterial pH should be monitored before infusion and after each 50-mEq dose (1 to 2 mEq/kg in children).

* Steroids may provide some benefit when bundled with vasopressin and epinephrine in treating IHCA (In-Hospital Cardiac Arrest). While routine use is not recommended pending follow-up studies, it would be reasonable for a provider to administer the bundle for IHCA.

Post-Cardiac Arrest Care
* ROSC After VF/pVT
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)

* Lidocaine: 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.
(While earlier studies showed an association between giving lidocaine after myocardial infarction and increased mortality, a recent study of lidocaine in cardiac arrest survivors showed a decrease in the incidence of recurrent VF/pVT but did not show either long-term benefit or harm.)

* ß-blocker: 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 ß-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT.
(There is inadequate evidence to support the routine use of a ß-blocker after cardiac arrest. However, the initiation or continuation of an oral or IV ß-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT.
Why: In an observational study of patients who had ROSC after VF/pVT cardiac arrest, ß-blocker administration was associated with higher survival rates. However, this finding is only an associative relationship, and the routine use of ß-blockers after cardiac arrest is potentially hazardous because ß-blockers can cause or worsen hemodynamic instability, exacerbate heart failure, and cause bradyarrhythmias. Therefore, providers should evaluate patients individually for their suitability for ß-blockers.)

Termination of CPR
* Low end-tidal carbon dioxide (ETCO ) 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 ETCO after 20 minutes of CPR in combination with other factors to help determine when to terminate resuscitation.

* ETCO for Prediction of Failed Resuscitation2
In intubated patients, failure to achieve an ETCO 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 ETCO 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 ETCO in determining when to terminate resuscitation.

Extracorporeal CPR
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.