Airway

Before tracheal intubation, the child’s airway can usually be managed effectively with bag-valve-mask (BVM) ventilation with proper head positioning and jaw thrust. Although tracheal intubation ensures optimal control of the airway for effective ventilation, multiple attempts at tracheal intubation by an inexperienced operator may seriously compromise the airway and increases the cumulative duration of “no flow” (i.e., no CPR) time.

In the child without an artificial airway, the use of BVM devices may result in a significant risk of gastric inflation, followed by pulmonary aspiration of gastric contents. Abdominal distention (gastric and bowel) can significantly compromise oxygenation; therefore the stomach should be vented when excessive gastric inflation occurs. One study found a 28% incidence of pulmonary aspiration in a series of failed resuscitations.¹⁶ For this reason as well as for the risk of barotrauma and volutrauma, excessive inflation pressures should be avoided. However, effective bilateral ventilation is best judged by visualizing bilateral chest excursions and listening to the quality of the breath sounds rather than setting a preset maximal inflation pressure.

Tracheal intubation should be performed as soon as appropriate personnel and equipment are available. The etco₂ is a valuable method of confirming correct placement of the tracheal tube. In the absence of capnography, a disposable colorimetric etco₂ device serves the same purpose. However, it is important to appreciate that etco₂ measurements are meaningful only in the presence of effective pulmonary circulation, such that a lack of color change may reflect either improper placement of the tube or a lack of pulmonary blood flow resulting from ineffective chest compressions or a massive pulmonary embolism. It is also essential to use the proper size colorimetric device for the child’s weight because the adult size may not detect the presence of CO₂ and may lead the user to misdiagnose a successful intubation.

Breathing

In the inpatient environment, equipment necessary to ventilate the lungs emergently should be readily available. Because the equipment provided for emergency ventilatory support may differ from standard equipment, depending on the location within a hospital, the anesthesiologist needs to be familiar with all of the equipment in the hospital in which he or she practices. Anesthesiologists are skilled providers of ventilatory support, but in the context of a cardiac arrest, must return to the basics and remember that if there is no chest movement, there is no ventilation. If no chest movement occurs during BVM ventilation despite an apparently good seal between the mask and the child’s face, the underlying cause, be it upper airway obstruction, whether anatomic or presence of a foreign body, bilateral tension pneumothoraces, or severe bronchospasm must be considered.

Overventilation is common during CPR, resulting in greater mean intrathoracic pressures than required, which decreases venous return and reduces cardiac output.¹⁷ In cardiopulmonary arrest, a less than normal minute ventilation may be appropriate, because cardiac output and delivery of CO₂ to the lungs are diminished. If an artificial airway is not in place for single person rescue, two breaths should be given for each 30 chest compressions. If an artificial airway is not in place for two person rescue, two breaths should be given after each 15 chest compressions. Once an artificial airway is in place, a ventilator rate of 8 to 10 per minute without pausing during rapid chest compressions should be used (Table 39-1).

Circulation

During cardiac arrest, chest compressions provide the sole perfusion to a child’s vital organs; therefore optimal performance of CPR is critical. Key elements to providing quality chest compressions include (1) ensuring an adequate rate (100 compressions per minute), (2) ensuring adequate chest wall depression (one third to half of the anteroposterior chest diameter), (3) releasing completely between compressions to allow full chest wall recoil, (4) minimizing interruptions in chest compressions, and (5) ensuring that the child is on a sufficiently hard surface to allow effective chest compressions.¹⁸ In short, push hard and push fast, release completely, and do not interrupt compressions unnecessarily. Incomplete recoil during CPR is associated with higher intrathoracic pressures and significantly decreased venous return, and coronary and cerebral perfusion.¹⁹

If a child is small enough (e.g., younger than 6 months) that the person providing chest compressions can comfortably encircle the chest with his or her hands, chest compressions should be performed using the circumferential technique, with thumbs depressing the sternum and the fingers supporting the infant’s back and circumferentially squeezing the thorax (Fig. 39-1). In larger infants, the sternum can be compressed using two fingers; and in the child, either one or two hands can be used, depending on the size of the child and of the rescuer.¹⁹ Whichever method is used, focused attention must remain on delivering effective compressions with minimal interruptions.²⁰ In all cases other than circumferential CPR, a backboard must be used. Properly delivered chest compressions are tiring to the provider, and providers should rotate approximately every 2 minutes to prevent compressor fatigue and deterioration in the quality and rate of chest compressions.¹⁹

FIGURE 39-1 Chest-encircling method for cardiac compressions in a neonate: thumbs are placed one finger’s breadth below the nipple line.

(Modified from Todres ID, Rogers MC. Methods of external cardiac massage in the newborn infant. J Pediatr 1975;86:781-2.)

Mechanisms of Blood Flow

External chest compressions provide cardiac output through two mechanisms: the cardiac pump mechanism and the thoracic pump mechanism. By the cardiac pump mechanism of blood flow, blood is squeezed from the heart by compression of the heart between the sternum and the vertebral column, exiting the heart only anterograde because of closure of the atrioventricular valves. Between compressions, ventricular pressure decreases below atrial pressure, allowing the atrioventricular valves to open and the ventricles to fill. This sequence of events resembles the normal cardiac cycle. Although the cardiac pump is likely not the dominant blood flow mechanism during most closed-chest CPR, specific clinical situations have been identified in which the cardiac pump mechanism is more prominent. For example, a smaller, more compliant chest may allow for more direct cardiac compression (Fig. 39-2). Increasing, the applied force during chest compressions also increases the likelihood of direct cardiac compression.

FIGURE 39-2 A, Cardiac pump mechanism by which the heart is directly squeezed between the sternum and vertebral column, representing artificial systole. B, Artificial diastole occurs with relaxation of the compressions.

(From Babbs CF. New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-5, © by Williams & Wilkins.)

Several observations do not support the cardiac pump as the primary mechanism of blood flow during CPR. Angiographic studies show that blood passes from the vena cava through the right heart into the pulmonary artery and from the pulmonary veins through the left heart into the aorta during a single chest compression.^21,22 Echocardiographic studies show that the atrioventricular valves are open during blood ejection.^21,23,24 Without closure of atrioventricular valves during chest compression, the cardiac pump mechanisms cannot account for forward movement of blood during CPR.

In 1976, Criley and colleagues²⁵ made the dramatic observation that several patients who developed ventricular fibrillation during cardiac catheterization produced enough blood flow to maintain consciousness by repetitive coughing.²⁵ The production of blood flow by increasing thoracic pressure without direct cardiac compression describes the thoracic pump mechanism, in which the heart is a passive conduit for blood flow. The intrathoracic pressure is greater than the extrathoracic pressure during the compression phase of CPR, at which time blood flows out of the thorax, with venous valves preventing excessive retrograde blood flow (Fig. 39-3). Experimental and clinical data support both mechanisms of blood flow during CPR in human infants.

FIGURE 39-3 A, Thoracic pump mechanism by which blood flow occurs through a general increase in intrathoracic pressure with external compressions (i.e., the heart is a passive conduit). B, Artificial diastole occurs with release of external compressions.

(From Babbs CF, New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-5, © by Williams & Wilkins.)

Electric Countershock

Electric countershock, or defibrillation, is the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia. Defibrillation should not be delayed to secure an airway, because the likelihood of restoring an organized rhythm decreases with increased duration of fibrillation. Ventricular fibrillation is terminated by simultaneous depolarization and sustained contraction of a critical mass of myocardium,²⁹ allowing return of spontaneous, coordinated cardiac contractions, assuming the myocardium is well oxygenated and the acid-base status is relatively normal. Drug treatment may be required as an adjunct to defibrillation, but by itself cannot be relied on to terminate ventricular fibrillation.

An older generation of defibrillators that is still present in many hospitals delivers energy in a monophasic damped sinusoidal waveform (Fig. 39-4, A). This type of instrument delivers a single, unidirectional current with a gradual decrease to zero current. By contrast, the newer generation of biphasic defibrillators delivers a current in a positive direction for a set period, followed by a reversal in current (see Fig. 39-4, B). Biphasic defibrillators are more effective than monophasic defibrillators in terminating ventricular fibrillation in adults; therefore their use is recommended where possible.

FIGURE 39-4 Energy delivery during conventional monophasic (A) and biphasic truncated exponential (B) defibrillation.

In the majority of adult cases, energy levels of 100 to 200 joules are successful when shocks are delivered with minimal delay.^30,31 The goal of defibrillation is to deliver a minimum of electrical energy to a critical mass of ventricular muscle while avoiding excessive current that could further damage the heart. The most reliable predictor of success of defibrillation is the duration of fibrillation before the first countershock.³² Acidosis and hypoxemia also decrease the success of defibrillation.³²

Practical Aspects of Defibrillation in Children

Correct paddle size and position are critical to the success of defibrillation. The largest paddle size appropriate for the child should be used because a larger size reduces the density of current flow, which in turn reduces myocardial damage. In general, adult paddles should be used in children weighing more than 10 kg and infant paddles should be used in infants weighing less than 10 kg. Paddle force is important as well. If the entire paddle does not rest firmly on the chest wall, a current of increased density will be delivered to a small contact point. Paddles should be positioned on the chest wall so that the bulk of myocardium lies directly between them. One paddle is placed to the right of the upper sternum below the clavicle; the other is positioned just caudad and to the left of the left nipple. For children with dextrocardia, the position of the paddles should be a mirror image. An alternative approach is to place one paddle anteriorly over the left precordium and the other paddle posteriorly between the scapulae.

The interface between the paddle and chest wall can be gel pads, electrode cream, or electrode paste. The electrode cream produces less impedance than the paste. Electric current follows the path of least resistance, so care should be taken that the interface material from one paddle does not touch that of the other paddle. This is especially important in infants, in whom the distance between paddles is small. If the gel is continuous between paddles, a short circuit is created and an insufficient amount of current will traverse the heart. Use of bare metal paddles increases the risk of arcing and worsens cutaneous burns from defibrillation. The use of self-adhesive pads is preferable when feasible.

In an oxygen (O₂)-enriched atmosphere, sparking from poorly applied defibrillator paddles can cause a fire. Therefore any sources of free-flowing O₂ should be removed to a distance of at least 1 meter from the child. These potentially hazardous O₂ sources include nasal cannula O₂, “blow-by” O₂, and nebulizers powered by O₂. By contrast, O₂ in a closed circuit may remain on the child. For example, it is not necessary to disconnect the ventilator from the child’s tracheal tube (if a ventilator is disconnected, the fresh gas flow should be turned off because large volumes of O₂ flow through disconnected ventilators).

For children with in-hospital ventricular fibrillation or pulseless ventricular tachycardia, defibrillation should be attempted as soon as possible, with optimal CPR until the defibrillator is ready to deliver a shock. For the first defibrillation attempt, 2 joules/kg of delivered energy should be administered (Fig. 39-5). After shock delivery, CPR should resume immediately with chest compressions for five duty cycles (2 minutes). If one shock fails to eliminate ventricular fibrillation, the incremental benefit of another immediate shock is small. Resumption of CPR is likely to confer a greater benefit than another shock. CPR may provide coronary perfusion, increasing the likelihood of defibrillation with a subsequent shock. It is important to minimize the time between chest compressions and shock delivery and between shock delivery and resumption of postshock compressions.²⁰ Approximately 2 minutes of CPR should be delivered before a second attempt at defibrillation at twice the original energy level (4 joules/kg).²⁰

FIGURE 39-5 Algorithm for diagnosis and treatment of acute cardiac dysfunction in the operating room. CPR, Cardiopulmonary resuscitation; ECG, electrocardiogram; PEA, pulseless electrical activity.

If ventricular fibrillation or pulseless ventricular tachycardia persists beyond the second defibrillation attempt, standard doses of epinephrine should be administered (with subsequent doses every 3 to 5 minutes during persistent cardiac arrest). After 2 minutes of chest compressions, defibrillation should be attempted again, followed by administration of amiodarone (5 mg/kg) or lidocaine (1 mg/kg) with subsequent defibrillation attempts. It is not necessary to increase the energy level on each successive shock during defibrillation after the second dose. However, successful defibrillation has been reported with currents in excess of 4 joules/kg without adverse sequelae, up to a maximum dose not exceeding 10 joules/kg or the adult level, whichever is less.²⁰ This sometimes occurs when a fixed energy level, adult automated external defibrillator (AED) is used in a small child.

Open-Chest Defibrillation

If the chest is already open in the OR or easily opened as in a fresh postoperative cardiac patient, ventricular fibrillation should be treated with open-chest defibrillation, using internal paddles applied directly to the heart. These should have a diameter of 6 cm for adults, 4 cm for children, and 2 cm for infants. Handles should be insulated. Saline-soaked pads or gauzes should be placed between the paddles and the heart. One electrode is placed behind the left ventricle and the other over the right ventricle on the anterior surface of the heart. The energy level used should begin at 5 joules in infants and 20 joules in adults.

Automated External Defibrillation

Use of AEDs is now standard therapy in out-of-hospital resuscitation of adults.^19,30 AEDs are now deemed appropriate for use in children older than 1 year. If available, use of pediatric attenuator pads or a pediatric mode on the AED should be used in children 1 to 8 years of age, but if unavailable (and a standard defibrillator is similarly unavailable), an unmodified AED should be used.

Transcutaneous Cardiac Pacing

In the absence of in situ pacing wires or an indwelling transvenous or esophageal pacing catheter, transcutaneous cardiac pacing (TCP) is the preferred method for temporary electrical cardiac pacing in children with asystole or severe bradycardia. TCP is indicated for children whose primary problem is impulse formation or conduction, with preserved myocardial function. It is most effective in those with sinus bradycardia or high-grade atrioventricular block, with slow ventricular response but adequate stroke volume. TCP is not indicated for children during prolonged arrest, because in this situation it usually results in electrical but not mechanical cardiac capture and its use may delay or interfere with other resuscitative efforts.

To set up pacing, one electrode is placed anteriorly at the left sternal border and the other posteriorly just below the left scapula. Smaller electrodes are available for infants and children, but adult-sized electrodes can be used in children weighing more than 15 kg. ECG leads should be connected to the pacemaker, the demand or asynchronous mode selected, and an age-appropriate heart rate used. The stimulus output should be set at zero when the pacemaker is turned on and then increased gradually until electrical capture is identified on the monitor. After electrical capture is achieved, whether an effective arterial pulse is generated must be determined. If not, additional resuscitative efforts should be initiated.

The most serious complication of TCP is the induction of a ventricular arrhythmia. Fortunately, this is rare and may be prevented by pacing only in the demand mode. Mild transient erythema beneath the electrodes is common. Skeletal muscle contraction can be minimized by using large electrodes, a 40-msec pulse duration, and the smallest stimulus required for capture. If defibrillation or cardioversion is necessary, a distance of 2 to 3 cm must be allowed between the electrode and paddles to prevent arcing of the current.

Vascular Access and Fluid Administration

One of the key aspects of successful CPR is early establishment of a route for administration of fluids and medications. If intravenous access cannot be established rapidly, the intraosseous or endotracheal route should be used (see Chapter 48).

Endotracheal Medication Administration

In the absence of other vascular access, medications including lidocaine, atropine, naloxone, and epinephrine (mnemonic LANE) can be administered via the endotracheal tube.^36,37 The use of ionized medications such as sodium bicarbonate or calcium chloride is not recommended by this route. The peak concentration of epinephrine or lidocaine administered via the endotracheal route may be less compared with the intraosseous route. For example, the peak drug concentration of epinephrine after endotracheal administration was only 10% of that after intravenous administration in anesthetized dogs. The recommended dose for epinephrine via the endotracheal tube is 10 times the intravenous or intraosseous dose or 0.1 mg/kg for bradycardia or pulseless arrest.

The volume and the diluent in which the medications are administered through an endotracheal tube may be important. When large volumes of fluid are used, pulmonary surfactant may be altered or destroyed, resulting in atelectasis. The total volume of fluid delivered into the trachea with each drug administered should not exceed 10 mL in children and 5 mL in infants and neonates.³⁸ However, administering an adequate volume of a drug is important to reach a large area of mucosal surface beyond the tip of the endotracheal tube for absorption. Absorption into the systemic circulation may be further enhanced by deep intrapulmonary administration by passing a catheter beyond the tip of the tracheal tube deep into the bronchial tree. The risk associated with the endotracheal route of drug administration is the formation of an intrapulmonary depot of drug, which may prolong the drugs’ effect. This could theoretically result in postresuscitation hypertension and tachycardia or the recurrence of fibrillation after normal circulation is restored.

Monitoring During Cardiopulmonary Resuscitation

A basic clinical examination is vital during cardiac arrest. The chest is carefully observed for adequacy of bilateral chest expansion with artificial ventilation and for equal and normal breath sounds. In addition, the depth of compression and the position of the rescuer’s hands should be constantly reevaluated in performing chest compressions by palpation of a major artery. Palpation is essential in establishing absence of a pulse and in assessing the adequacy of blood flow during chest compressions. Palpating the peripheral pulses may be inaccurate, especially during intense vasoconstriction associated with the use of epinephrine.

An indwelling arterial catheter, when available, is a valuable monitor in assessing the arterial blood pressure. Specific attention should be paid to diastolic blood pressure as it relates directly to adequacy of coronary perfusion during CPR. In addition, arterial access allows for frequent blood sampling, particularly for measurement of arterial pH and blood gases. Pulse oximetry can be used during CPR to determine the O₂ saturation and may be of value in assessing the adequacy of cardiac output, as reflected in the plethysmograph. The ECG can suggest metabolic imbalances and diagnose electrical disturbances.

The etco₂ monitor provides important information during the course of resuscitation. Because the generation of exhaled CO₂ depends on pulmonary blood flow, it can provide a useful indicator of the adequacy of cardiac output generated by chest compressions. As the cardiac output increases, the ETco₂ increases and the difference between end-tidal and arterial CO₂ becomes smaller.³⁹ In animal models, etco₂ during CPR correlates with coronary perfusion pressure and with ROSC.^40,41 In adults during cardiac arrest, an etco₂ greater than 10 mm Hg is positively associated with ROSC and hospital survival.^42,43 When the etco₂ is less than 10 mm Hg, efforts should be taken to enhance the quality of chest compressions (push hard, push fast, release completely, minimize interruptions, and optimize hand position). A reduced etco₂ may occur transiently in the presence of adequate chest compressions after administration of epinephrine owing to an increase in intrapulmonary shunting.

Temperature should be monitored during and after CPR. The resuscitation of the child with hypothermia as the cause of cardiac arrest must be continued until the child’s core temperature exceeds 95° F (35° C). A glass bulb thermometer measures the temperature to very low values. Repeated measurements of core body temperature should be made at several sites (rectal, bladder, esophageal, axillary, or tympanic membrane) where possible, to avoid misleading temperature readings from a single site, because local body temperature may vary with changes in regional blood flow during CPR. Hyperthermia should be aggressively treated in the periarrest period, because postarrest hyperthermia is associated with worse outcomes in children.⁴⁴ Evidence suggests a benefit to induced hypothermia after resuscitation from cardiac arrest in adults^45,46 and after perinatal hypoxic or ischemic injury.⁴⁷ The data available to support the use of hypothermia in infants and children after cardiac arrest is from case series and retrospective studies. Pending results of a randomized controlled trial (Therapeutic Hypothermia After Pediatric Cardiac Arrest), clinicians may choose to control a child’s temperature in the range of 91.4° to 95° F (33° to 35° C) for 12 to 48 hours after resuscitation with slow subsequent rewarming (see section on Postresuscitation Stabilization).

α- and β-Adrenergic Agonists

In 1963, only 3 years after the original description of closed-chest CPR, Redding and Pearson⁴⁸ demonstrated that early administration of epinephrine in a canine model of cardiac arrest improved the success rate of CPR. They also demonstrated that the increase in aortic diastolic pressure with the administration of α-adrenergic agonists was responsible for the improved success of resuscitation. They theorized that vasopressors such as epinephrine were of value because the drug increased peripheral vascular tone and, hence, coronary perfusion pressure. The relative importance of α- and β-adrenergic agonist actions during resuscitation has been widely investigated. In a canine model of cardiac arrest, only 27% of dogs that received a pure β-adrenergic receptor agonist along with an α-adrenergic antagonist were resuscitated successfully, compared with 100% of dogs that received a pure α-adrenergic agonist and a β-adrenergic antagonist. Other investigators have demonstrated that the α-adrenergic effects of epinephrine resulted in intense vasoconstriction of the resistance vessels of all organs of the body, except those supplying the heart and brain.⁴⁹ Because of the widespread vasoconstriction in nonvital organs, adequate perfusion pressure and thus blood flow to the heart and brain can be achieved despite the fact that cardiac output is very low during CPR.^49–51

The increase in aortic diastolic pressure associated with epinephrine administration during CPR is critical for maintaining coronary blood flow and enhancing the success of resuscitation.^52,53 Even though the contractile state of the myocardium is increased by the use of β-adrenergic agonists in the spontaneously beating heart, β-adrenergic agonists may actually decrease myocardial blood flow by increasing intramyocardial wall pressure and vascular resistance during CPR.⁵⁴ By its inotropic and chronotropic effects, β-adrenergic stimulation increases myocardial O₂ demand, which, when superimposed on low coronary blood flow, increases the risk of ischemic injury.

Any medication that causes systemic arterial vasoconstriction can be used to increase aortic diastolic pressure and resuscitate the heart. For example, pure α-adrenergic agonists can be used in place of epinephrine during CPR. Phenylephrine and methoxamine, two α-adrenergic agonists, have been used in animal models of CPR with success equal to that of epinephrine. Their use results in a greater O₂ supply to demand ratio in the ischemic heart and at least a theoretical advantage over the combined α- and β-adrenergic agonist effects of epinephrine. These agonists, as well as other classes of vasopressors such as vasopressin, have been used successfully for resuscitation.

The merits of using a pure α-adrenergic agonist during CPR have been questioned by some investigators. Although the inotropic and chronotropic effects of β-adrenergic agonists may have deleterious hemodynamic effects during CPR for ventricular fibrillation, increases in both heart rate and contractility will increase cardiac output when spontaneous coordinated ventricular contractions are achieved.

Epinephrine

Epinephrine (adrenaline) is an endogenous catecholamine with potent α- and β-adrenergic stimulating properties. The α-adrenergic action increases systemic and pulmonary vascular resistance, increasing both systolic and diastolic blood pressure. The increase in diastolic blood pressure directly increases coronary perfusion pressure, thereby increasing coronary blood flow and increasing the likelihood of ROSC.^52,53 The β-adrenergic effect increases myocardial contractility and heart rate and relaxes smooth muscle in the skeletal muscle vascular bed and bronchi. Epinephrine also increases the vigor and intensity of ventricular fibrillation, increasing the likelihood of successful defibrillation.⁵⁵

Larger than necessary doses of epinephrine may be deleterious. Epinephrine may worsen myocardial ischemic injury secondary to increased O₂ demand and may result in postresuscitative tachyarrhythmias, hypertension, and pulmonary edema. Epinephrine causes hypoxemia and an increase in alveolar dead space ventilation by redistributing pulmonary blood flow.^39,56 Prolonged peripheral vasoconstriction by excessive doses of epinephrine may delay or impair reperfusion of systemic organs, particularly the kidneys and gastrointestinal tract.

Routine use of large-dose epinephrine in in-hospital pediatric cardiac arrest should be avoided. A randomized, controlled trial in 2003 compared high-dose with standard-dose epinephrine for children with in-hospital cardiac arrest refractory to initial standard-dose epinephrine. Survival was reduced at 24 hours, with a trend toward decreased survival to hospital discharge in the children who received large doses of epinephrine.⁵⁷ Despite these data, large doses of epinephrine may be considered in special cases (e.g., β-blocker overdose), particularly when diastolic blood pressure remains low despite excellent chest compression and several standard doses of epinephrine.

Vasopressin

Vasopressin is a long-acting endogenous hormone that causes vasoconstriction (V1 receptor) and reabsorption of water in the renal tubule (V2 receptor). In experimental models of cardiac arrest, vasopressin increases blood flow to the heart and brain and improves long-term survival compared with epinephrine.^58,59 In a randomized trial comparing the efficacy of epinephrine to vasopressin in shock-resistant out-of-hospital ventricular fibrillation in adults, vasopressin produced a greater rate of ROSC.⁶⁰ In a study of in-hospital adult cardiac arrest, vasopressin produced a rate of survival to hospital discharge similar to that of epinephrine.⁶¹

In a pediatric porcine model of prolonged ventricular fibrillation, the use of vasopressin and epinephrine in combination resulted in greater left ventricular blood flow than either vasopressor alone, and both vasopressin alone and vasopressin plus epinephrine resulted in superior cerebral blood flow than epinephrine alone.⁶² By contrast, in a pediatric porcine model of asphyxial cardiac arrest, ROSC was more likely in piglets treated with epinephrine than in those treated with vasopressin.⁶³ Pediatric^64–66 case series and reports suggested that vasopressin⁶⁴ or its long-acting analog, terlipressin,^65,66 may be effective in refractory cardiac arrest. In a 2009 National Registry of Cardiopulmonary Resuscitation (NRCPR) review, vasopressin was associated with reduced ROSC and a trend toward reduced 24-hour and discharge survival. There is insufficient evidence to make a recommendation for its routine use during cardiac arrest.²⁰

Atropine

Atropine, a parasympatholytic agent, blocks cholinergic stimulation of the muscarinic receptors in the heart, increasing the sinus rate and shortening atrioventricular node conduction time. Atropine may activate latent ectopic pacemakers. Atropine has little effect on systemic vascular resistance, myocardial perfusion pressure, or contractility.⁶⁷

Atropine is indicated for the treatment of asystole, pulseless electrical activity, bradycardia associated with hypotension, second- and third-degree heart block, and slow idioventricular rhythms. Atropine is particularly effective in clinical conditions associated with excessive parasympathetic tone. However, for children with asystole or symptomatic bradycardia associated with severe hypotension, epinephrine is the medication of choice and atropine should be regarded as a second-line drug.

The recommended pediatric dose of atropine is 0.02 mg/kg, with a maximum dose of 2 mg. The increase in heart rate after intravenous atropine (20 µg/kg) in infants and children may be attenuated compared with that in adults.⁶⁸ Although a minimum dose of 0.1 mg has been entrenched in the literature, it is not evidence-based.^68,69 Atropine may be given by any route, including intravenous, intraosseous, endotracheal, intramuscular, and subcutaneous. After intravenous administration, its onset of action is within 30 seconds and its peak effect occurs in 1 to 2 minutes. The recommended adult dose is 0.5 mg every 3 to 5 minutes until the desired heart rate is obtained, up to a maximum of 3 mg.

Sodium Bicarbonate

The routine use of sodium bicarbonate during CPR remains controversial, and it remains American Heart Association Class Indeterminate. Acidosis may depress myocardial function, prolong diastolic depolarization, depress spontaneous cardiac activity, decrease the electrical threshold for ventricular fibrillation, and reduce the cardiac response to catecholamines.^70–72 Acidosis also vasodilates systemic vessels and attenuates the vasoconstrictive response of peripheral vessels to catecholamines,⁷³ which is the opposite of the desired vascular effect during CPR. In children with a reactive pulmonary vascular bed, acidosis causes pulmonary hypertension. Therefore correction of even mild acidosis may be helpful in resuscitating children with increased pulmonary vascular resistance. Additionally, the presence of severe acidosis may increase the threshold for myocardial stimulation in a child with an artificial cardiac pacemaker.⁷⁴ Other situations in which administration of bicarbonate is indicated include tricyclic antidepressant overdose, hyperkalemia, hypermagnesemia, or sodium channel blocker poisoning.

Potentially deleterious effects of bicarbonate administration include metabolic alkalosis, hypercapnia, hypernatremia, and hyperosmolality. In a 2004 multicenter cohort study of in-hospital pediatric cardiac arrest, the use of sodium bicarbonate was associated with increased mortality.¹⁵ Alkalosis causes a leftward shift of the oxyhemoglobin dissociation curve and thus impairs release of O₂ from hemoglobin to tissues at a time when O₂ delivery may already be reduced.⁷⁵ Alkalosis also can result in hypokalemia by enhancing potassium influx into cells and in ionic hypocalcemia by increasing protein binding of ionized calcium. The marked hypercapnic acidosis that occurs during CPR in the venous circulation, including the coronary sinus, may be exacerbated by the administration of bicarbonate.⁷⁶ Myocardial acidosis during cardiac arrest is associated with decreased myocardial contractility.⁷² Hypernatremia and hyperosmolality may decrease tissue perfusion by increasing interstitial edema in microvascular beds.

Paradoxical intracellular acidosis after bicarbonate administration can occur with the rapid entry of CO₂ into cells with a slow egress of hydrogen ions out of cells; however, in neonatal rabbits recovering from hypoxic acidosis, bicarbonate administration increased both arterial pH and intracellular brain pH as measured by nuclear magnetic resonance spectroscopy.^77,78 Likewise, in rats, intracellular brain adenosine triphosphate concentration did not change during severe intracellular acidosis in the brain produced by extreme hypercapnia.⁷⁸ In a separate animal study, bicarbonate slowed the rate of decrease of both arterial and cerebral pH during prolonged CPR, suggesting that the blood-brain pH gradient is maintained during CPR.⁷⁹ Given the potentially deleterious effects of bicarbonate administration, its use should be limited to cases in which there is a specific indication, as discussed earlier.

Calcium

Calcium administration during CPR should be restricted to cases with a specific indication for calcium (e.g., hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdose). These restrictions are based on the possibility that exogenously administered calcium may worsen ischemia-reperfusion injury. Intracellular calcium overload occurs during cerebral ischemia by the influx of calcium through voltage-dependent and agonist-dependent (e.g., N-methyl-d-aspartate [NMDA]) calcium channels. Calcium plays an important role in the process of cell death in many organs, possibly by activation of intracellular enzymes such as nitric oxide synthase, phospholipase A and C, and others.⁸⁰

The calcium ion is essential in myocardial excitation-contraction coupling, in increasing ventricular contractility, and in enhancing ventricular automaticity during asystole. Ionized hypocalcemia is associated with decreased ventricular performance and the peripheral blunting of the hemodynamic response to catecholamines.^81,82 Severe ionized hypocalcemia has been documented in adults suffering from out-of-hospital cardiac arrest⁸² and in animals during prolonged CPR.⁸³ Thus children at risk for ionized hypocalcemia should be identified and treated as expeditiously as possible. Both total and ionized hypocalcemia may occur in children with either chronic or acute disease. Ionized hypocalcemia also occurs during massive or rapid transfusion of blood products (particularly whole blood and fresh frozen plasma) because citrate and other preservatives in stored blood products rapidly bind calcium. Because of this effect, ionized hypocalcemia is a known cause of cardiac arrest in the OR and should be treated immediately with calcium chloride or calcium gluconate (see Chapter 10). The magnitude of hypocalcemia in this setting depends on the rate and volume of blood products administered and the hepatic and renal function of the child. Administration of fresh frozen plasma at a rate in excess of 1 mL/kg/min significantly decreases the ionized calcium concentration in anesthetized children.⁸⁴

The pediatric dose of calcium chloride for resuscitation is 20 mg/kg with a maximum dose of 2 g. Calcium gluconate is as effective as calcium chloride in increasing the ionized calcium concentration.^85,86 The dose of calcium gluconate should be three times that of calcium chloride (milligram per kilogram,) (i.e., 20 mg/kg calcium chloride is equivalent to 60 mg/kg calcium gluconate), with a maximum dose of 2 g in children. Calcium should be given slowly through a large-bore, free-flowing intravenous cannula, or preferably a central venous line. When administered too rapidly, calcium may cause bradycardia, heart block, or ventricular standstill. Severe tissue necrosis occurs when calcium infiltrates into subcutaneous tissue. Calcium administration is not recommended for pediatric cardiopulmonary arrest in the absence of documented hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or hyperkalemia (Class III, level of evidence [LOE] B). Routine calcium administration in cardiac arrest provides no benefit and may be harmful.^74,87

Glucose

The administration of glucose during CPR should be restricted to children with documented hypoglycemia because of the possible detrimental effects of hyperglycemia on the brain during or after ischemia. The mechanism by which hyperglycemia exacerbates ischemic neurologic injury may be due to an increased production of lactic acid in the brain by anaerobic metabolism. During ischemia under normoglycemic conditions, brain lactate concentration reaches a plateau. In a hyperglycemic milieu, however, brain lactate concentration continues to increase for the duration of the ischemic period.⁸⁸

Clinical studies have shown a direct correlation between the initial post–cardiac arrest serum glucose concentration and poor neurologic outcome,^89–92 although the greater glucose concentration may be a marker rather than a cause of more severe brain injury.⁹⁰ However, given the likelihood of additional ischemic and hypoxic events in the postresuscitation period, it seems prudent to maintain serum glucose concentrations within the normal range. Additional studies are needed to determine if the benefit from tight control of serum glucose after cardiac arrest outweighs the risk of iatrogenic hypoglycemia. Some groups of children, including preterm infants and debilitated children with small endogenous glycogen stores, are more prone to developing hypoglycemia during and after a physiologic stress such as surgery. Bedside monitoring of the serum glucose concentration is critical during and after a cardiac arrest and allows for the opportunity to administer glucose before the critical point of small substrate delivery has been reached. The dose of glucose generally needed to correct hypoglycemia is 0.5 g/kg given as 5 mL/kg of 10% dextrose in infants or 1 mL/kg of 50% dextrose in an older child. The osmolarity of 50% dextrose is approximately 2700 mOsm/L and has been associated with intraventricular hemorrhage in neonates and infants; therefore the more dilute concentration is recommended in infants.

Amiodarone

Amiodarone has now supplanted lidocaine as the first drug of choice for medical management of shock-resistant ventricular tachycardia and fibrillation. The role of amiodarone was established for cardiac arrest after a series of studies showed it to be more effective than lidocaine in the management of refractory tachyarrhythmias in adults. Compared with lidocaine, amiodarone results in an increased rate of survival to hospital admission in patients with shock-resistant out-of-hospital ventricular fibrillation.⁹³

Early reports on the use of oral amiodarone in children were favorable.^94–96 Recent data on amiodarone use in children are limited to case reports and descriptive case series. Nevertheless, it is now used widely for serious pediatric arrhythmias in the nonresuscitation environment and appears to be effective and have an acceptable short-term safety profile.

The pharmacology of amiodarone is complex and may explain the wide range of its usefulness. It is primarily classified as a Vaughn-Williams class III agent that blocks the adenosine triphosphate–sensitive outward potassium channels causing prolongation of the action potential and refractory period; however, this effect requires intracellular accumulation. On intravenous loading, the antiarrhythmic effects are primarily due to noncompetitive α- and β-adrenergic receptor blockade, calcium channel blockade, and effects on inward sodium current causing a decrease in anterograde conduction across the atrioventricular node and an increase in the effective atrioventricular refractory period. The α-adrenergic blockade leads to vasodilation, which may increase coronary blood flow. It is poorly absorbed orally, requiring intravenous loading in urgent situations. The full antiarrhythmic impact requires a loading period of up to 1 to 3 weeks to achieve intracellular levels and full potassium channel–blocking effects.

Hypotension is commonly reported with intravenous administration and may limit the rate at which the drug can be given; however, the development of hypotension is less common with the newer, aqueous formulation.⁹⁷ The overall hemodynamic impact of intravenous administration will depend on the balance of its effect on rate control, myocardial performance, and vasodilation. Dosage recommendations for children are based on limited clinical studies. The dose is extrapolated from data on adults; 5 mg/kg intravenously for life-threatening arrhythmias. This dose can be repeated if necessary to control the arrhythmia. Intravenous loading doses are followed by a continuous infusion of 10 to 20 mg/kg/day if there is a risk of arrhythmia recurrence. The ideal rate of bolus administration is unclear; in adults, once diluted, it is given as an intravenous push. It is best administered over 20 to 60 minutes to avoid profound vasodilation. We recommend slow intravenous push (2 to 3 minutes) for pulseless ventricular tachycardia or ventricular fibrillation until the arrhythmia is controlled and then a slower bolus (up to 10 minutes) for the remainder of the dose. An alternative dosing regimen for children is 1 mg/kg intravenous push every 5 minutes up to 5 mg/kg. The use of the small aliquot bolus technique may be particularly appropriate for infants younger than 12 months of age.

Amiodarone-induced torsades de pointes has been described.⁹⁸ The use of amiodarone should be avoided in combination with other drugs that prolong the QT interval, as well as in the setting of hypomagnesemia and other electrolyte abnormalities that predispose to torsades de pointes. Severe bradycardia and heart block have also been described, especially in the postoperative period, and ventricular pacing wires are recommended in this setting. Both amiodarone and inhalation anesthetic agents prolong the QT interval; however, no specific data exist to evaluate the use of amiodarone for ventricular arrhythmias in children receiving inhalation anesthetics. It would seem prudent to be especially vigilant for this adverse effect in this circumstance.

Noncardiac adverse effects are often seen, especially with chronic dosing.⁹⁹ The most serious of these has been the development of interstitial pneumonitis seen most commonly in patients with preexisting lung disease.¹⁰⁰ The incidence in children is unknown. Rarely, an acute illness similar to acute respiratory distress syndrome illness has been reported in both infants and adults at the initiation of treatment.¹⁰¹ The lung disease may remit with early discontinuation of the drug. Hypothyroidism, hepatotoxicity, photosensitivity, and corneal opacities are also common side effects with chronic use.⁹⁹

Lidocaine

Lidocaine is a class IB antiarrhythmic that decreases automaticity of pacemaker tissue that prevents or terminates ventricular arrhythmias as a result of accelerated ectopic foci. Lidocaine abolishes reentrant ventricular arrhythmias by decreasing the action potential duration and the conduction time of Purkinje fibers and increases the effective refractory period of Purkinje fibers, reducing the nonuniformity of contraction. Lidocaine has no effect on atrioventricular nodal conduction time, so it is ineffective in the treatment of atrial or atrioventricular junctional arrhythmias. In healthy adults, no change in heart rate or blood pressure occurs with lidocaine administration. In patients with cardiac disease there may be a slight decrease in ventricular function when a lidocaine bolus is administered intravenously.

In children with normal cardiac and hepatic function, an initial intravenous bolus of 1 mg/kg of lidocaine is given, followed by a continuous intravenous infusion at a rate of 20 to 50 µg/kg/min. If the arrhythmia recurs, a second intravenous bolus at the same dose can be given. In children with severely decreased cardiac output, a bolus of no greater than 0.75 mg/kg is administered, followed by an infusion at the rate of 10 to 20 µg/kg/min. In children with hepatic disease, dosages should be decreased by 50%. Children with renal insufficiency have normal lidocaine pharmacokinetics; however, toxic metabolites may accumulate in children receiving infusions over a long period. In children with hypoproteinemia, the dose of lidocaine also should be lowered, because of the increase in free fraction of the drug.

Toxic effects of lidocaine occur when the serum concentration exceeds 7 to 8 µg/mL and include seizures, psychosis, drowsiness, paresthesias, disorientation, agitation, tinnitus, muscle spasms, and respiratory arrest. The treatment of choice for lidocaine-induced seizures is a benzodiazepine (midazolam or lorazepam) or a barbiturate (e.g., phenobarbital; chronic therapy also increases the hepatic metabolism of lidocaine).¹⁰² Conversion of second-degree heart block to complete heart block has been described,¹⁰³ as has severe sinus bradycardia. Lidocaine is not as effective as amiodarone for improving ROSC or survival to hospital admission among adults with ventricular fibrillation refractory to ventricular fibrillation and shock.¹⁰⁴

Perioperative Cardiac Arrest

The incidence, causes, and risk factors associated with anesthesia- and operative-related cardiac arrest have been evaluated by the Pediatric Perioperative Cardiac Arrest registry.^105,106 Cardiovascular causes of cardiac arrest were the most common (41% of all arrests), with hypovolemia from blood loss and hyperkalemia from transfusion of stored blood the most common identifiable cardiovascular causes. Among respiratory causes of arrest (27%), airway obstruction from laryngospasm was the most common cause. Vascular injury incurred during placement of central venous catheters was the most common equipment-related cause of arrest. The cause of arrest varied by phase of anesthesia care.

Cardiac arrest in the OR should have the greatest potential for a successful outcome, because it is a witnessed arrest with virtually instantaneous availability of skilled personnel, monitoring equipment, resuscitative equipment, and drugs. Whenever a cardiac arrest occurs in the OR, the circumstances causing the arrest should be rapidly determined. The circumstances of the arrest may provide a clue as to the cause, such as hyperkalemia after succinylcholine administration or rapid blood transfusion, hypocalcemia during a rapid infusion of fresh frozen plasma or large blood transfusion, or a sudden fall in etco₂ indicating air, blood clot, or tumor embolism. A bradyarrhythmia always must be assumed to be first resulting from hypoxemia; second, caused by anesthetic overdose (real or relative); and third, possibly related to a vagal reflex caused by surgical or airway manipulation. Administering 100% O₂ and ensuring adequate ventilation is always the first maneuver, regardless of the cause of the bradycardia. In reflex-induced bradycardia, atropine may be the first drug of choice, but in extreme cases of bradycardia, whatever the mechanism, epinephrine should be used. Hypotension and a low cardiac output state must be rapidly corrected by appropriate administration of intravenous fluids, vasopressors, and adequate chest compressions to circulate drugs to have the needed clinical effect. Once chest compressions are required, the standard American Heart Association recommendations for CPR generally apply and this includes the frequent administration of epinephrine. Figure 39-5 presents an algorithm for the differential diagnosis and treatment of the more common causes of acute OR-associated cardiac dysfunction.

Hyperkalemia

A child with a hyperkalemic cardiac arrest may be identified by history, by the progression of ECG changes leading up to the arrest, or by initial laboratory results. A high index of suspicion must be maintained for hyperkalemia as a cause of cardiac arrest because it requires specific therapy. Along with the usual resuscitation algorithms, immediate therapy to antagonize the effects of an increased serum potassium level is necessary. Calcium gluconate or calcium chloride will antagonize the effects of hyperkalemia at the myocardial cell membrane, increasing the threshold for fibrillation. Sodium bicarbonate and hyperventilation will increase the serum pH and shift potassium from the extracellular to the intracellular compartment; insulin (with concomitant dextrose) will also cause potassium to shift intracellularly (0.1 unit/kg of insulin with 0.5 g/kg of dextrose; 2 mL/kg of dextrose 25%). The serum potassium concentration must be monitored frequently during this treatment, preferably by point-of-care testing modalities. Because these therapies shift potassium intracellularly, therapy to remove potassium from the body (furosemide, hemodialysis, sodium polystyrene sulfonate) also may be indicated.

Anaphylaxis

Anaphylaxis is an unusual, but usually reversible, cause of cardiac arrest. Manifestations of anaphylaxis include skin reaction (usually flushing, pallor, or urticaria), airway edema and possible obstruction, bronchospasm, and cardiovascular collapse. Anaphylaxis may be particularly severe in situations of decreased endogenous catecholamines, such as in a child taking β-blockers or in children receiving spinal or epidural anesthesia.

Resuscitation of the child with anaphylaxis rests on reversing airway obstruction and restoring intravascular volume and vascular tone. In the child with cardiac arrest, standard-dose epinephrine should be administered intravenously. In the child with impending cardiac arrest, 0.01 mL/kg of subcutaneous epinephrine (1 : 1000 concentration) may be preferred. Children with anaphylactic shock have profound intravascular depletion requiring rapidly administered, large-volume fluid resuscitation (20 mL/kg boluses). In addition to the usual resuscitation medications, treatment should include an antihistamine and corticosteroid, such as diphenhydramine (Benadryl), 1 mg/kg, and methylprednisolone (Solu-Medrol) 2 mg/kg. Inhaled bronchodilators such as albuterol may help reverse bronchospasm. If severe airway obstruction occurs, endotracheal intubation or even cricothyroidotomy may become difficult or impossible. Therefore the airway should be secured early on by a skilled practitioner.

Supraventricular Tachycardia

Supraventricular tachycardia (SVT), a common arrhythmia in infants and children, may be associated with severe circulatory compromise or even cardiac arrest. Therapy for this arrhythmia should be based on the child’s hemodynamic status. SVT associated with inadequate circulation should be treated immediately with synchronized cardioversion beginning at a dose of 0.5 J/kg. If intravenous access is available, adenosine can be administered while cardioversion is being prepared; however, cardioversion should not be delayed while intravenous access is being obtained.

Adenosine is the medical treatment of choice for SVT. The underlying mechanism in children is usually a reentry circuit involving the atrioventricular node. Adenosine causes a temporary block in the atrioventricular node and interrupts this reentry circuit. The initial dose is 0.1 mg/kg given as a rapid intravenous bolus. Central venous administration is preferable because the drug is rapidly metabolized by red blood cell adenosine deaminase and therefore has a half-life of only 10 seconds. When the drug is given peripherally, the intravenous line should be immediately and rapidly flushed with 10 mL of saline. If there is no interruption in the reentry circuit, successive doses of 0.2 and 0.4 mg/kg should be given. In neonates, a smaller initial dose of 0.05 mg/kg is given and increased by 0.05 mg/kg/dose until termination of the arrhythmia up to a maximum dose of 0.3 mg/kg.¹⁰⁷ When SVT appears without any circulatory compromise, conversion of the arrhythmia may first be attempted with a vagal maneuver such as ice to the face. If this is ineffective, then adenosine should be utilized.

Other medications used to treat SVT have a greater incidence of adverse effects than adenosine. Digoxin is often ineffective and causes frequent arrhythmias. Verapamil should be avoided in infants because of its association with congestive heart failure and cardiac arrest because of its negative inotropic effects.¹⁰⁸ Flecainide is effective in treating SVT but has many cardiac and noncardiac adverse effects¹⁰⁹; its role for hemodynamically unstable SVT remains to be established. Other therapies include β-adrenergic blockers, edrophonium, and α-agonists. If SVT persists despite medical therapy and the child progresses to circulatory instability, electrical cardioversion should proceed immediately.

Pulseless Electrical Activity

Pulseless electrical activity (PEA) is defined as organized ECG activity, excluding ventricular tachycardia and fibrillation, without clinical evidence of a palpable pulse or myocardial contractions. It may occur spontaneously after cardiac arrest or as an intervening rhythm associated with treatment for cardiac arrest. The causes of PEA is divided into primary (cardiac) and secondary (noncardiac) causes. Primary PEA, associated with cardiac arrest, is due to depletion of myocardial energy stores and thus responds poorly to therapy. Drugs used to treat primary PEA include epinephrine, atropine, calcium, and sodium bicarbonate.

The causes of secondary PEA are often remembered using the 4 Hs and 4 Ts mnemonic: hypovolemia, hypoxia, hypothermia, and hypo- or hyper-electrolytemia (hyperkalemia, hypocalcemia), tension pneumothorax, pericardial tamponade, thromboembolism, and toxins (anesthetic overdose). In secondary PEA, intervention is directed at the underlying disorder and usually results in a successful resuscitation. When the cause of PEA is unknown and the child does not respond to medications, giving a fluid bolus and inserting needles into the pleural space to rule out pneumothorax and into the pericardial space to rule out cardiac tamponade should considered.

Open-Chest Cardiopulmonary Resuscitation

The use of open-chest cardiac massage, although generally replaced by closed-chest CPR, still has an active role in the OR and ICU especially during and after thoracic surgery. Compared with closed-chest CPR, open-chest CPR generates greater cardiac output and vital organ blood flow. During open-chest CPR, less elevation occurs in intrathoracic, right atrial, and intracranial pressure, resulting in greater coronary and cerebral perfusion pressure and greater myocardial and cerebral blood flow.^110–112

Typically, in the OR and ICU, open-chest CPR is preferable to closed-chest CPR in the child who has had a recent sternotomy. Open-chest CPR is also indicated for selected children when closed-chest CPR has failed, although exactly which children should receive this method of resuscitation under this condition is controversial. When initiated early after failure of closed-chest CPR, open-chest CPR may improve outcome.^113–115 When performed after 15 minutes of closed-chest CPR, open-chest CPR significantly improves coronary perfusion pressure and the rate of successful resuscitation.¹¹⁶

Extracorporeal Membrane Oxygenation

In institutions with the ability to rapidly mobilize an extracorporeal circuit, extracorporeal cardiopulmonary bypass (CPB) should be considered for refractory pediatric cardiac arrest when the condition leading to arrest is reversible and when the period of no flow (cardiac arrest without CPR) was brief. Survival with a good neurologic outcome is possible after more than 50 minutes of CPR in selected children who were resuscitated via extracorporeal CPB.^117,118 CPB requires major technical support and sophistication but can be rapidly implemented in hospitals set up to do so. However, absence of a formal rapid deployment extracorporeal membrane oxygenation (ECMO) team does not preclude resuscitation ECMO in pediatric cardiac patients with good results.¹¹⁹ Extracorporeal CPB should be reserved for children who have effective CPR initiated immediately after cardiac arrest.

Active Compression-Decompression

Active compression-decompression CPR uses a negative-pressure “pull” on the thorax during the release phase of chest compression using a handheld suction device. This technique has been shown to improve vascular pressures and minute ventilation during CPR in animals and humans.^120–124 The hemodynamic benefit of this technique is attributed to enhancement of venous return by the negative intrathoracic pressure generated during the decompression phase. Thus, when this technique was used with a device adding impedance to inspiration, vascular pressures and flow increased further.¹²⁵ Its effectiveness in adults shows promise, with increased survival and a trend toward neurologic improvement in prehospital victims.^126–128 However, two recent, larger trials did not demonstrate improved survival in in-hospital or prehospital victims of cardiac arrest, nor did any subgroup demonstrate benefit from active compression-decompression CPR.^129–131 The complication rate, including fatal rib and sternal fractures, may be greater with this technique.¹³²