The American Heart Association's 300-page treatise updating the ACLS guidelines covers everything from where a patient should go after a field arrest to recommendations for post-cardiac arrest care. The organization made minimal changes, however, to pediatric advance life support guidelines, contending that the same approach works for all ages — essentially, chest compressions first. The updated guidelines do, however, simplify the approach to all individuals with sudden death, and can increase bystander CPR.
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Field JM, et al
2010;122(18 Suppl 3):S639
It is axiomatic that most pediatric cardiac arrests are from asphyxia, rarely from primary ventricular fibrillation or tachycardia (VF/VT). The pathway is usually asphyxia, systemic hypoxia, hypercapnia, and acidosis, with bradycardia and hypotension culminating in cardiac arrest. VF accounts for only five percent to 15 percent of all inpatient and outpatient pediatric cardiac arrests, and although it is rare in young children, its incidence increases with age. In an athletic event, for example, the AHA recommends that a witnessed sudden cardiac arrest should be treated as VF, with emphasis on adult-like chest compression and early defibrillation.
The AHA now promulgates chest compression-only for the initial resuscitation of adults in cardiac arrest. Ventilation is secondary, and not initially required for optimal, albeit still poor, results. Although chest compression is still strongly supported for all age groups, resuscitation of infants or toddlers is best accomplished by a combination of ventilation and chest compressions, rather than by chest compressions alone. In fact, compression-only CPR in an asphyxial pediatric arrest has results no better than arrests with no bystander CPR. (Lancet 2010;375:1347.)
The AHA deals separately with newborns, infants, and children. The depth of compression in children is from 1.5 to 2 inches at a rate of 30:2 (compressions:breaths) with a continued emphasis on pushing hard and fast, and allowing the chest to completely recoil after each compression. It is estimated that starting with compressions first loses only about 18 seconds of ventilation time, so compress the chest immediately while preparing for rescue breathing in children. For neonates, however, traditional ABC is the preferred sequence because such arrests are almost always respiratory in origin.
Other minor additions to the new guidelines include the endorsement of cuffed endotracheal tubes for infants and children. The initial defibrillation shock of 2-4 J/KG remains.
Because of the potential harm of high-concentration oxygen exposure after cardiac arrest, using 100% oxygen for newborn-neonatal codes should be limited, and prolonged hyperoxemia should be avoided in all cases. This is counterintuitive for most clinicians, and many would reach for and continue 100% oxygen post-arrest in any circumstance. I'm not sure this concept will be maintained, but limiting the use of 100% oxygen post-cardiac arrest is a new and interesting take on post-resuscitative care for children and adults. To be specific, room air alone, eschewing supplemental oxygen, is a new recommendation for resuscitation of preterm infants. It is instructive to note that healthy term babies normally start life at a hemoglobin saturation less than 60%, and it normally takes more than 10 minutes to reach a saturation more than 90%. The theory is that hyperoxemia is unnatural and may be toxic, especially in preterm infants. The AHA recommends that babies born at term should receive room air rather than 100% oxygen. This is quite a change from my medical school days.
Suctioning newborns is also deemphasized because no evidence confirms that airway suction in active babies is helpful, even with meconium in the airway. The downside is that prolonged suctioning produces bradycardia and vasodilation. Bottom line: Don't give 100% oxygen to healthy newborns, and throw away the suctioning bulb as a routine intervention in vigorously breathing infants. Reasonable suctioning is still supported (“insufficient evidence to support a change”) in the newborn with respiratory distress.
In newborns, the recommended compression:ventilation ratio remains at 3:1, emphasizing that ventilation is critical to the newborn asphyxial arrest. Based on positive experience in adults, therapeutic hypothermia is recommended as post-cardiac arrest care for resuscitated children with coma. I doubt that many clinicians are aware of this recommendation or have been following it. I am not sure how it would be best done, and it has not yet been studied to any extent.
The AHA provides comment on the ethics of resuscitation of newborns. It is considered appropriate to stop resuscitative efforts if there is no detectable heartbeat after only 10 minutes. With obvious congenital abnormalities or birth weights that are associated with early death or unacceptably high morbidity in the rare survivor, the AHA states that “resuscitation is not indicated.” The AHA defines extreme prematurity, a contraindication to resuscitation, as a gestational age of less than 23 weeks. Again, I doubt that many clinicians are aware of these recommendations, and continue to resuscitate newborns much longer than 10 minutes. The AHA briefly discusses the concept of prolonged codes for tissue and organ transplantation.
Bag-valve-mask ventilation is considered effective and maybe even safer than ET ventilations for short periods of infant cardiac arrest. The ability of the paramedic to intubate a young child quickly and efficiently — and correctly — in the field is limited, and many EMS systems have totally abandoned attempting prehospital intubation for young children.
Vascular access can be either via a peripheral vein or an intraosseous (IO) needle. IO access is supported in cardiac arrest for infants and children because it produces drug levels almost as rapidly as venous administration. Endotracheal drug administration is acceptable for lidocaine, epinephrine, atropine, and naloxone. The optimal drug dosage for endotracheal administration is unknown and empiric. In general, it appears reasonable to double or triple the intravenous dose when administering the drugs by the tracheal tube.
Bicarbonate and calcium should not be given through the ET tube. As with adults, however, no medication has been found to alter the outcome of cardiac arrest in infants and children, so most of the information or recommendations on drug dosing during cardiac arrest are simply an educated guess. The AHA does not recommend routine immediate venous access as an initial route for drugs or fluid during cardiac arrest. Certainly, one should not waste an inordinate amount of time attempting to cannulate a peripheral vein during cardiac arrest. Instead, concentrate on the basics of chest compressions and ventilations.
The guidelines spend a significant amount of time on well known medications for asystole and various arrhythmias in cardiac arrest in infants and children. The interested reader can consult the full text.
The overall survival-to-discharge rate from out-of-hospital cardiac arrest in infants and children has been somewhat stagnant for more than 20 years: about three percent for infants and nine percent for children and adolescents. Children and infants are much less likely to survive an out-of-hospital cardiac arrest than adults. Survival from inhospital cardiac arrest for infants and children is somewhat more sanguine: 25 percent to 30 percent.
Other miscellaneous concepts are advanced. The AHA says capillary refill time alone is a poor indicator of circulatory volume, and can be influenced by ambient temperature, age, and available lighting. While we all seem to focus and comment on the mysterious capillary refill time, it's real clinical value is obtuse. While mentioned in many textbooks and omnipresent on chart documentation, capillary refill is likely an inconsequential physical finding for making change in critical care. Concerning ventilation pressures, children are susceptible to vigorous overventilation during cardiac arrest, resulting in markedly elevated intrathoracic pressure. This quickly impairs venous return and reduces cardiac output as well as cerebral and coronary blood flow. Air trapping from excessive ventilation may further impede return of spontaneous circulation. The neophyte's natural instinct to rapidly and forcibly ventilate an arrested child is counterproductive.
As with adults, there is insufficient evidence to recommend routine cricoid pressure to prevent aspiration during ET intubation in children. Cricoid pressure may be quite detrimental to delivering oxygenation in the child compared with the larger airways of an adult.
Sudden Unexplained Deaths
The 2010 AHA guidelines address sudden unexplained deaths in infants and children. The well-known SIDS deaths and rarer sudden death in older children and young adults may be associated with genetic mutations of ion channels, termed cardiac channelopathies. This is a relatively new concept, but with a cardiac channelopathy, abnormal movement of electrolytes across cell membranes predispose the heart to arrhythmias. Such mutations may be found in up to 10 percent of cardiac arrest victims and in as many as 20 percent of young adults with sudden death in whom the cause is not evident by a routine autopsy. (Not highlighted is the fascinating Brugada syndrome as a cause of sudden death in adolescents. Available in the EMN archive: 2009;31:9; http://bit.ly/EMNbrugada.)
When sudden unexplained cardiac arrest occurs in a seemingly normal and well conditioned adolescent, especially athletes, think VF. The amateur is tempted to consider foul play or drug use. I would caution you to keep these thoughts to yourself until further information is forthcoming. An incriminating prior EKG may give a hint of Brugada syndrome, but these are usually not available. Channelopathy tests are still nascent investigations but a fascinating concept. The AHA recommends that all infants, children, and adults with sudden unexpected cardiac death have an unrestricted autopsy by a pathologist with training and expertise in cardiovascular pathology, particularly looking for genetic issues and the channelopathies.
Next month's column will discuss some specific ACLS scenarios, and how intervention should be tailored for such issues as drug OD, asthma, and renal failure.
Comments about this article? Write to EMN at email@example.com.
Click and Connect!Access the links in this article by reading it onwww.EM-News.com.
Tracheal Intubation in Infants and Children
Although it's best for the unskilled clinician to first use bag-valve-mask ventilation for pediatric arrest, both cuffed and uncuffed tubes are now acceptable for intubating infants and children in cardiac arrest, another new concept for the seasoned clinician from the AHA. The difficulty in selecting the proper sized uncuffed tube is somewhat mitigated by using the cuffed device, and complications are no greater comparing cuffed with noncuffed tubes. Aspiration may be less with a cuffed ET tube. Selecting the appropriate size tube is recommended with this formula:
Uncuffed ET tube ID diameter (mm) = 4 + (age/4)
Cuffed ET ID diameter (mm) = 3.5 + (age/4)
Correct tube placement consists of:
- Observing bilateral chest movement.
- Auscultating equal breath sounds over both lung fields, especially in the axilla.
- Lack of gastric insufflation sounds over the stomach.
- Measurement of exhaled CO2 by a variety of monitors.
- Pulse oximetry.
- A chest x-ray to identify proper position in the mid-trachea.
- Visual confirmation that the tube was placed through the cord by the initial attempt or with subsequent laryngoscopy.
It is noted that small tubes can be easily obstructed or displaced by simply flexing or extending of the child's neck. A pneumothorax can be produced from vigorous bagging in a small child.
Part 2 in a Series
Time to Turn Back the Valve on the Oxygen Tank?
Is oxygen a toxin to infants and post-cardiac arrest adults? Perhaps, according to the AHA. Although one might intuit that maximal oxygenation is best post-code, or for anyone after cardiac arrest, this long-held axiom has been recently challenged.
Although it is reasonable and still recommended to ventilate with 100% oxygen during CPR, because the optimal inspired concentration under these circumstances is unknown, once circulation is restored, it may be time to turn back the valve on the oxygen tank.
Hemoglobin saturation of greater than 94% is considered adequate oxygenation by the AHA for anyone post-cardiac arrest, with a goal of avoiding prolonged hyperoxemia. For adults, it is currently suggested to decrease the post-resuscitation-inspired oxygen concentration to less than 100% as long as the oxyhemoglobin saturation can be maintained at greater than 94%. The concept of high oxygen exposure after cardiac arrest as being of potential harm is an important, albeit somewhat inscrutable, change in the 2010 AHA guidelines. Theoretically, high-dose oxygen facilitates the generation of oxygen derived free radicals during brain reperfusions. This may increase brain lipid peroxidation, increase metabolic dysfunction, increase neurological degeneration, and therefore produce a worse final outcome.
Note that finding 100% saturation on a pulse oximeter can correspond to PaO2 anywhere between 80 mm Hg and 500 mm Hg, leading to the recommendation that the clinician be satisfied with a 94% reading on the oximeter and resist the urge to keep it at 100%. To be specific, room air alone, eschewing supplemental oxygen, is a new recommendation for resuscitation of preterm infants. It is instructive to note that healthy term babies normally start life at a hemoglobin saturation less than 60%, and it normally takes more than 10 minutes to reach a saturation more than 90%, giving rise to the theory that hyperoxemia can be toxic, especially in preterm infants. The AHA recommends that babies born at term receive room air rather than 100% oxygen.
I'm not sure why the AHA decided to warn doctors about the possible detrimental effects of 100% oxygen post-cardiac arrest. This may be overthinking it or a recommendation not yet ready for prime time. Traumatic brain injury and ischemic strokes seem to have pathophysiology somewhat related to sudden cardiac arrest with regard to brain damage. In these circumstances, the mechanism that underlies brain death is thought to occur in the poorly perfused penumbral areas.
Maximizing oxygen delivery, rather than limiting it, has been advocated as an important and effective modality in treating traumatic brain injury (TBI). Even hyperbaric oxygen has been touted to be beneficial post-stroke and post-brain injury. I am completely confused about the benefit or harm of oxygen post-cardiac arrest. Interested readers should try to understand a review by CM Tolias. (Transfusion Alter Transfusion Med 2010;11:148.)
This article, delivered to thousands of doctors over the Medscape emergency medicine website, touts the benefit of oxygen for TBI and acute ischemic stroke, seemingly a direct contradiction to the AHA's view of limiting supplemental oxygen post-cardiac arrest. I remain totally flummoxed by the discussion and the diametrically opposed views on the use of oxygen.