1

What is the etiology of cardiac arrest in children?

Most cardiac arrest events in infants and children are precipitated by respiratory failure or shock. Sudden cardiac arrest may be observed less frequently. Typically, sudden cardiac arrest is the result of an arrhythmia, such as pulseless VT or VF. Genetic mutations resulting in channelopathies have been linked to sudden cardiac arrest, such as in sudden infant death syndrome and sudden death in children. Channelopathies are a group of diseases that are characterized by abnormal myocyte ion channels or the proteins that regulate them resulting in fatal arrhythmias.

Primary factors that may lead to cardiac arrest in pediatric patients are respiratory failure, shock, and sudden arrhythmias (pulseless VT or VF). Secondary factors that may contribute to cardiac arrest and should be considered when managing arrest victims are listed in Box 83-1 .

2

How do survival rates from cardiac arrest differ when comparing in-hospital with out-of-hospital settings?

Infants and children who experience in-hospital cardiac arrest are more likely to survive the event than infants and children in the out-of-hospital setting. However, overall there remains room for improvement in this area. For the most part, the numbers are low for infants and children who survive to discharge from the hospital after in-hospital (33%) or out-of-hospital (4%–13%) cardiac arrest. The American Heart Association (AHA) maintains an ongoing focus on early recognition and rapid intervention of respiratory failure or shock to prevents progression to cardiac arrest. When cardiac arrest occurs, early recognition and high-quality cardiopulmonary resuscitation (CPR) are important to improve survival.

3

What changes occurred to pediatric chest compression depth and compression/ventilation ratios with the 2010 american heart association guidelines?

A major change in the 2010 AHA Guidelines is to begin CPR with chest compressions as opposed to providing breaths. With this in mind, the initial “look, listen, and feel for breathing,” was eliminated. For many of us who learned the phrase “airway, breathing, and circulation (A-B-C),” it now has become “circulation, airway, and breathing (C-A-B).” The reason for this change was to prevent delayed chest compressions even though the most common origin of cardiac arrest in pediatrics is of a respiratory nature. The impetus for this change is multifactorial, as follows:

• •
  

  Because high-quality chest compressions are the basis for effective CPR, time to initiation of chest compressions is important to survival. The time to deliver two breaths, particularly by nonskilled providers, delays chest compressions for a greater period of time (>18 seconds) than would the delay to first breath (≤18 seconds) if chest compressions are performed initially. Even though respiratory causes of cardiac arrest are more likely in pediatric populations, the time to first breath would not be significantly delayed.

  
  
• •
  

  A bystander who is not a skilled health care provider may be more inclined to initiate CPR with chest compressions than rescue breaths. Because of this, the AHA has advocated for a number of years “hands-only” (chest compression–only) CPR for the bystander who is reluctant to perform rescue breathing. A bystander providing only chest compressions is better than not performing CPR at all.

  
  
• •
  

  For the ease of learning CPR, especially for unskilled providers, the C-A-B sequence, although better suited for adult victims, is taught for both adult and pediatric resuscitation.

The 2010 recommendation for chest compression depth (“push hard”) is approximately one third of the anterior-posterior diameter of the chest wall. This correlates with approximately 1.5 inches (4 cm) for an infant and 2 inches (5 cm) for a child ( Table 83-1 ). Full chest recoil should occur between chest compressions.

During cardiac arrest, it is crucial that chest compressions are performed early and effectively without frequent or prolonged interruptions to generate a better cardiac output. To some extent, the cardiac output provides essential organs with much needed blood flow to restore baseline circulation as close as possible. Cycles of CPR should continue uninterrupted for 2 minutes before checking for a rhythm and pulse and should resume within 10 seconds. The number of compressions per minute changed from 100 to at least 100 compressions per minute (“push fast”). During resuscitation by more than one health care provider, the person doing chest compressions should change after each 2-minute cycle because fatigue is associated with lower quality chest compressions.

4

What are the recommendations for the delivery of breaths with and without an advanced airway?

Without an advanced airway (e.g., endotracheal tube, laryngeal mask airway), breaths should be synchronized with chest compressions. Two breaths are given after 30 compressions (30:2) with one rescuer and after 15 chest compressions (15:2) with two rescuers. Each breath should not last >1 second and should be terminated when chest rise is detected (see Table 83-1 ). Excessive ventilation interferes with cardiac output and coronary artery perfusion. Excessive ventilation also could cause gastric distention, which would increase the risk of aspiration.

With an advanced airway, breaths and chest compressions are asynchronous. One breath is given every 6–8 seconds (i.e., 8–10 breaths per minute). Care must be taken to avoid excessive ventilation by terminating inflation when chest rise is achieved.

When an endotracheal tube is placed during resuscitation, capnography should be used to confirm placement. If possible, continuous monitoring of end-tidal carbon dioxide (ETCO ₂ ) should be used during CPR as an indirect measure of the quality of chest compressions. An ETCO ₂ of at least 10–15 mm Hg is associated with effective cardiac compressions. Return of spontaneous circulation (ROSC) is associated with increased ETCO ₂ , usually to >40 mm Hg.