Chapter 20: Cardiopulmonary Resuscitation

• The code leader must ensure high-quality cardiopulmonary resuscitation (CPR) be integrated into advanced life-support measures in order to ensure a good outcome during resuscitation.

• Chest compressions should be initiated before ventilations in order to immediately provide blood flow to the heart and brain (2010 AHA C-A-B recommendations).

• When two or more health care providers are performing CPR in an infant or child, the correct compression-to-ventilation ratio is 15:2 (15 compressions followed by 2 ventilations). In all other circumstances, the ratio is 30:2.

• Two-minute cycles of CPR should be performed before stopping compressions to reassess the child.

• Automated external defibrillators (AEDs) can now be safely and effectively used in infants and children of all ages. If possible use a pediatric attenuator device for children weighing less than 25 kg.

• Ventricular fibrillation and pulseless ventricular tachycardia are treated with single shocks followed immediately by 2-minute cycles of CPR in order to maintain myocardial perfusion after each defibrillation.

• Length-based tapes facilitate medication dosing and device size selection.

• Intraosseous (IO) lines can be used in any age for an IV medication.

• IV or IO medication administration is preferred over the endotracheal route.

• Pulseless electrical activity (PEA) requires the identification and correction of reversible causes, the most common of which is hypovolemia. Consider a rapid fluid bolus in any child presenting in a PEA rhythm.

• The quality of chest compressions can be monitored with continuous monitoring of end-tidal CO₂. Less than 10 to 15 mm Hg may indicate low cardiac output during CPR, whereas >10 to 15 mm Hg suggests effective chest compressions during CPR. An abrupt rise in end-tidal CO₂ (ETCO₂) during chest compressions may suggest the return of spontaneous circulation.

• After the return of spontaneous circulation, avoid the risk of hyperoxia reperfusion injury. Titrate the oxygen FiO₂ administration to maintain oxygen saturations of 94% to 99%.

Sudden cardiac arrest due to a primary cardiac dysrhythmia is rare in children.¹ Unrecognized and progressive respiratory distress and shock are the most common etiologies of cardiopulmonary arrest (CPA) in children. The outcome for out-of-hospital CPA is poor with only 4% to 13% of children surviving to hospital discharge.² The survival rate of in-hospital CPA is approximately 27% to 33%.^2,3 Early recognition of a child in respiratory distress and/or compensated shock (Chapters 17,18,19) is essential to prevent the progression to CPA.

The 2010 AHA CPR and PALS guidelines continue to emphasize the importance of high-quality cardiopulmonary resuscitation (CPR) by lay rescuers and by health care providers. The major change regarding the sequence of actions for CPR in the 2010 AHA guidelines is the “C-A-B” sequence, which stands for “compressions–airway–breathing.”⁴ This new emphasis on initiating chest compressions before ventilations provides for more immediate perfusion to the heart and brain. Immediate chest compressions can be initiated much faster than opening the airway and providing ventilations. The delay in providing assisted ventilations when using C-A-B is approximately 18 seconds when the 30:2 compression-to-ventilation ratio is used, and shorter when the 15:2 compression-to-ventilation ratio is being used in infants and children.⁴

Table 20-1 lists the five essential components of high-quality chest compressions.⁶ The universal compression to ventilation ratio for one-rescuer CPR in any age victim is 30:2. When there are two health care providers performing CPR, the compression to ventilation ratio for infants and children is 15:2. The effectiveness of CPR is measured by palpable pulses during cardiac compressions. Overzealous ventilations during CPR may be harmful by decreasing venous return to the heart and limiting cardiac output. The major points of emphasis in the 2010 PALS guidelines are noted in Table 20-2.

Although uncuffed endotracheal tubes (ETTs) have traditionally been used in pediatric patients, cuffed ETTs may be safely used in the hospital setting in children younger than 8 years (except for the newly born) under certain circumstances such as poor lung compliance, high airway resistance, or a large glottic leak.⁷ The cuff pressure must be monitored and kept <20 cm H₂O.

Although laryngeal mask airways (LMAs) have been extensively used by pediatric anesthesiologists in the operating room, there is currently insufficient evidence to recommend the routine use of LMAs in children during cardiac arrest.⁷ However, if a child in CPA cannot be adequately ventilated and oxygenated via bag-mask techniques and if intubation attempts have failed, an LMA can be used during CPR.

Once an advanced airway has been inserted, confirm proper tube placement and proper ventilation by clinical assessment and confirmatory devices. Check for adequate and symmetric rise and fall of the chest. The colorimetric CO₂ detector is commonly used to confirm tracheal intubation. There are several false-positive and false-negative conditions that may occur when using a colorimetric CO₂ detector device. During CPA, the lungs are poorly perfused resulting in insufficient exhaled CO₂ to register on the detector despite correct tracheal intubation. Adult-sized CO₂ detectors used in infants might similarly be falsely negative. Children who have consumed carbonated beverages just prior to intubation may have enough carbon dioxide present in their stomachs to produce a color change during an esophageal intubation. Avoid this false-positive condition by providing six ventilations prior to attaching a CO₂ detector device to check for the presence of exhaled carbon dioxide.

Following intubation, provide 8 to 10 ventilations per minute during CPR. Excessive ventilations during CPR can impede venous return potentially compromising cardiac output during CPR.⁸

During the resuscitation, the clinician must continuously reassess the adequacy of ventilations via the ETT. Clinical deterioration suggests ETT complications which can be quickly and systematically assessed via the “DOPE” mnemonic.⁹

• D = Dislodged or displaced ETT (esophageal intubation or right mainstem displacement)

• O = Obstructed ETT (kinked tube or internal obstruction with blood, mucus, and/or emesis)

• P = Pneumothorax (tension)

• E = Equipment failure (disconnected tubing, too small ETT with air leak, and/or inadequate volume of ventilations)

Intravenous (IV) or intraosseous (IO) access is the preferred method of medication administration during any resuscitation. Although a few medications (i.e., “L-A-N-E” = lidocaine, atropine, naloxone, and epinephrine) can be administered via the ETT during a resuscitation, lower blood concentrations result when administered via the ETT which may produce adverse transient β-effects (hypotension and lower coronary perfusion pressure).⁷ In infants and younger children, the preferred IO site is the flat-medial portion of the proximal tibia (i.e., 2–3 cm below the tibial tuberosity). An alternative site for older children is the distal tibia (i.e., 2–3 cm proximal to the medial malleolus). Any medication that can be given via the IV route can also be administrated via the IO route in all ages.

Estimation of a Child's Weight for Medication Administration

Difficulties encountered during a pediatric resuscitation include medication calculations, which are always based on a child's weight, and selection of appropriate-size equipment (i.e., ETT, IV catheter sizes, chest tube sizes). Parent and physician weight estimations can be error prone. One quick method for estimating a child's weight is based on the child's age and can be reviewed in Table 20-3.¹⁰

Length-based weight estimation tapes (i.e., Broselow tape) are recommended by PALS. They also calculate medication doses and device sizes reducing the potential for errors. The validity of length-based tapes has been re-verified in recent studies.^11,12 A previous study claims that a length-based tape inaccurately estimated the actual weight in up to one-third of children.¹³ There are some weight estimate error concerns raised for obese and cachectic children. The addition of body habitus assessments to length-based systems has demonstrated more accurate weight estimations.¹⁴

A systematic approach to pediatric dysrhythmia stabilization and management depends on two key clinical factors:

1. Does the child have a pulse?

2. If a pulse is present, is the child hemodynamically stable or unstable and what is the child's heart rate?

All of the 2010 PALS dysrhythmia treatment algorithms can be summarized into one treatment algorithm (Fig. 20-1). Children who present with a dysrhythmia but who exhibit good perfusion parameters including strong distal pulses, brisk capillary refill, and warm extremities, may not require any emergent interventions unless the presenting rhythm has the potential to degenerate into a more serious condition. Children who exhibit ECG evidence of conduction abnormalities (i.e., Mobitz type II second-degree heart blocks, complete heart blocks, prolonged QT intervals or aberrant conduction such as the Wolff–Parkinson–White syndrome) may also warrant more emergent treatment.¹⁵ In infants, prearrest rhythm disturbances can manifest as fussiness, lethargy, poor feeding, pallor, respiratory distress, or as cardiogenic shock. In older children, it may present as chest pain, palpitations, difficulty breathing, or syncope.

The most common pediatric arrest rhythms that will confront the emergency physician are asystole and bradyasystole. Ventricular fibrillation (VF) and ventricular tachycardia (VT) are less common; however, some infants and children are at a higher risk of developing various primary cardiac dysrhythmias¹⁵ (Table 20-4).

The four pulseless rhythms that will be addressed in this chapter can be clinically divided into two general categories based on their similar treatment approaches:

1. Shockable rhythms: VF and pulseless ventricular tachycardia (PVT)

2. Nonshockable rhythms: Asystole and pulseless electrical activity (PEA)

VF and PVT require defibrillation followed immediately by CPR. Asystole and PEA require CPR, epinephrine, and a search for reversible causes. Regardless of the presenting arrest rhythm, the emergency physician must also place a high priority on finding the underlying etiology or etiologies which may have led to the arrest rhythm. The 11 reversible causes of CPA that are emphasized in the 2010 PALS guidelines can be remembered as the “six Hs and five Ts” (hypovolemia, hypoxemia, hypoglycemia, hypothermia, hypo/hyperkalemia, hydrogen ion excess, tension pneumothorax, tamponade-cardiac, toxins, thrombosis—pulmonary, and thrombosis—cardiac).¹⁶ Another useful mnemonic to quickly remember the most common reversible causes of PEA in children is “P-A-T2-H4”¹⁵ (Table 20-5).

The 2010 PALS guidelines recommend the use of continuous monitoring of ETCO₂ to monitor the quality of chest compressions. An ETCO₂ <10 to 15 mm Hg may indicate low cardiac output during CPR. An ETCO₂ >10 to 15 mm Hg suggests effective chest compressions during CPR. An abrupt rise in ETCO₂ during chest compressions may suggest a return of spontaneous circulation.¹⁷

Paroxysmal supraventricular tachycardia (PSVT) is the most common symptomatic dysrhythmia in infants and children. Infants with PSVT typically present with nonspecific symptoms such as fussiness, lethargy, tachypnea, pallor, and/or difficulty feeding. Although infants can generally tolerate PSVT episodes with heart rates in the 200 to 300 beats/minute range, if left untreated, they may develop congestive heart failure and/or shock. Older children with PSVT typically complain of palpitations, difficulty breathing, and/or vague chest discomfort. The QRS complex width in pediatric PSVT is most commonly a narrow complex rhythm. Wide complex PSVT is less common but may be seen in a child with a preexisting bundle branch block or in a child with an antidromic reentry phenomenon, in which the conduction from the atria initially goes down to the ventricles via an accessory pathway and then returns retrograde from the ventricles back to the atria from the atrioventricular (AV) node.

The management of PSVT depends on the child's hemodynamic stability and availability of IV access (Tables 20-6 and 20-7).¹⁸ A continuous rhythm strip should be recorded during any conversion attempt. Hemodynamically stable PSVT in infants and young children can be initially treated with ice applied to the face. A plastic bag or surgical glove filled with a slurry of crushed ice and water can be applied over the infant's forehead, eyes, and bridge of the nose for approximately 10 to 15 seconds. Care must be taken to avoid occluding the infant's nostril and mouth during this maneuver. Older children may be asked to submerge their face in a basin of cold water in addition to trying other vagal maneuvers listed in Table 20-6. Failure to convert following vagal maneuvers and IV adenosine requires pediatric cardiology consultation, elective cardioversion, and/or other medications such as amiodarone or procainamide. Verapamil should be avoided in infants and younger children because of the high incidence of profound hypotension and cardiovascular collapse when this medication is administered in this age group. Immediate cardioversion should be performed in any infant or child who exhibits PSVT with significant hemodynamic instability.

Symptomatic Bradycardia

Bradydysrhythmias are the most common prearrest rhythms in children and are usually associated with severe hypoxemia, hypotension, and metabolic acidosis. Other reversible causes of bradycardia include hypothermia, hyperkalemia, toxins, and heart blocks.¹⁹ Bradycardia is poorly tolerated in infants and children because they are not physiologically capable of increasing their stroke volume to maintain an adequate cardiac output. Clinically significant bradycardia is defined as a heart rate lower than the normal rate for age and it is associated with clinical signs of poor systemic perfusion. Chest compressions should be initiated for an absolute heart rate <60 beats/minute that is associated with clinical signs of poor systemic perfusion.

The first step in the management of symptomatic bradycardia is to ensure adequate oxygenation and ventilation because hypoxia is the most common etiology of bradycardia in children. Children who remain symptomatic despite adequate oxygenation and ventilation will require chest compressions and medications to convert the bradycardia. Although atropine is the first-line medication to treat symptomatic bradycardia in adult patients, epinephrine is the first medication of choice to treat symptomatic bradycardia in children that is unresponsive to adequate oxygenation and ventilation. Because the efficacy of epinephrine is reduced in the face of hypoxia and acidosis, ensure adequate ventilation, oxygenation, and chest compressions/perfusion²⁰ (Tables 20-6 and 20-7). Atropine would be indicated before epinephrine if the etiology of the child's bradycardia was felt to be due to an increase in vagal tone, cholinergic toxicity, or AV blocks.²¹ Other etiologies to consider include hypothermia, increased intracranial pressure, heart blocks (congenital and acquired), a denervated heart status—postcardiac transplant, hypothyroidism, sick sinus syndrome, and various medications and toxins such as digoxin, β-blockers, calcium-channel blockers, and cholinergic toxicity. Consider emergency pacing for Mobitz type II second-degree AV blocks, complete AV blocks, or sick sinus syndrome.

VT is an uncommon pediatric dysrhythmia. The majority of children with VT have underlying conditions that predispose them to developing VT such as postcardiac surgery, myocarditis, cardiomyopathies, and prolonged QT syndrome. Electrolyte abnormalities (hyperkalemia, hypocalcemia, and hypomagnesemia) and drug toxicities (cyclic antidepressants and cocaine) must also be considered.¹⁵ The treatment of a child with VT and a pulse will be dependent on the child's hemodynamic stability (Tables 20-6 and 20-7). Torsades de pointes is a unique type of polymorphic VT that deserves special consideration. Prolonged QT syndrome, hypomagnesemia, underlying cardiac defects, and various medications (cyclic antidepressants and calcium-channel blockers) have all been implicated as known causes of torsades de pointes. Procainamide and amiodarone are both contraindicated in the treatment of torsades because both of these antidysrhythmic agents are capable of prolonging the QT interval, which could then cause a further deterioration of the torsades rhythm. Lidocaine may be the preferred medication to treat VT that is caused by a drug-induced prolongation of the QT interval.

Ventricular Fibrillation and Pvt

VF and PVT (pulseless VT) were previously thought to occur very rarely in pediatric CPA cases. However, in a previous study of in-hospital cardiac arrest, a shockable rhythm was present during some point of the resuscitation in 25% of the cases.³ VF and PVT should also be suspected as the initial arrest rhythm in cases of commotiocordis and in cases of witnessed sudden cardiac arrest in children. The treatment approach to VF and PVT was significantly revised in the 2005 PALS guidelines. The sequence of actions of defibrillations followed immediately by 2-minute cycles of CPR is again emphasized in the 2010 PALS guidelines. Once VF or PVT is identified, defibrillation maneuvers should be immediately followed by 2-minute cycles of CPR.²² Rhythm checks and pulse checks should only be performed after 2-minute cycles of CPR. Although a single shock by a biphasic defibrillator has a high likelihood of terminating VF, the resulting rhythm is typically a nonperfusing rhythm that therefore requires CPR in order to maintain perfusion to the heart and brain until normal cardiac contractility can resume.²³ Epinephrine is administered with the second defibrillation maneuver (and can be repeated every 3–5 minutes). An antidysrhythmic agent (amiodarone) is administered with the third defibrillation maneuver. Although the sequence of actions (defibrillations followed by immediate CPR) and recommended medications (epinephrine and antidysrhythmics) for shockable rhythms have not changed since the 2005 PALS guidelines, the 2010 PALS guidelines recommend 4 to 10 J/kg (not to exceed the adult maximum) for the third and subsequent shocks.²²

Asystole is the most common pulseless arrest rhythm presenting to the emergency department (ED). The survival rate for children who present to the ED in asystole is dismal. Tables 20-6 and 20-7 summarize the treatment of asystole and PEA. Children who present to the ED in PEA have a slightly higher chance of survival compared with those children who present in asystole. The underlying cause of PEA must be determined and if not corrected, the child will not survive. Since profound hypovolemia is the most common etiology of PEA in children, one should always consider a rapid fluid bolus. The various etiologies of PEA are listed in Table 20-5. In addition to a very focused history and physical examination, a bedside measurement of pH, PaO₂, potassium, ionized calcium, and hematocrit can quickly assist the emergency physician in ruling out various etiologies of PEA.

Special circumstances such as trauma, drowning, toxins and anaphylaxis can all precipitate cardiopulmonary arrest in children. The specific management issues in these special circumstances are covered in other chapters throughout this book. Although a detailed description of postresuscitation care is beyond the scope of this chapter, several key points should be kept in mind. One of the major points of emphasis in the 2010 PALS postresuscitation guidelines is to reduce the risk of reperfusion injury by avoiding hyperoxia. Once return of spontaneous circulation has been achieved, titrate the oxygen FiO₂ administration to maintain an oxygen saturation of 94% to 99%. Avoid oxygen saturations of 100% postresuscitation since an oxygen saturation of 100% may correspond to a PaO₂ of approximately 80 to 500 mm Hg.²⁴ Avoid hyperthermia and treat fever aggressively. Consider the use of vasoactive medications in the postresuscitation phase because myocardial depression commonly exists in those children who survive the initial resuscitation. Avoid the routine use of hyperventilation in the postresuscitation phase unless the patient is exhibiting signs of impending cerebral herniation. Treat postresuscitation seizures aggressively and search for an underlying etiology such as hypoglycemia and various other electrolyte disturbances. Patients who remain comatose during the postresuscitation period may neurologically benefit from a brief period of hypothermia at 32°C to 34°C for 12 to 24 hours.²⁵ Because glucose is the major metabolic substrate for the neonatal myocardium, untreated hypoglycemia can depress neonatal myocardial function.²⁶ A quick and easy method to rapidly calculate and administer 0.5 g/kg of IV dextrose for hypoglycemia is listed in Table 20-8.²⁷