Introduction
In contrast to adults, sudden cardiac arrest in children is uncommon, and cardiac arrest does not usually result from a primary cardiac cause. More often it is the terminal event of progressive respiratory failure or shock, also called an asphyxial arrest.

Respiratory Failure
Respiratory failure is characterized by inadequate ventilation or oxygenation. Anticipate respiratory failure and possible respiratory arrest if you see any of the following:
• An increased respiratory rate, particularly with signs of distress (eg, increased effort, nasal flaring, retractions, or grunting)
• An inadequate respiratory rate, effort, or chest excursion (eg, diminished breath sounds, gasping, and cyanosis), especially if mental status is depressed.

Shock
Shock results from inadequate blood flow and oxygen delivery to meet tissue metabolic demands. Shock progresses over a continuum of severity, from a compensated to a decompensated state. Attempts to compensate include tachycardia and increased systemic vascular resistance (vasoconstriction) in an effort to maintain cardiac output and blood pressure. Although decompensation can occur rapidly, it is usually preceded by a period of inadequate end-organ perfusion.

Signs of compensated shock include:
• Tachycardia
• Cool extremities
• Prolonged capillary refill (despite warm ambient temperature)
• Weak peripheral pulses compared with central pulses
• Normal blood pressure

As compensatory mechanisms fail, signs of inadequate end-organ perfusion develop. In addition to the above, these signs include
• Depressed mental status
• Decreased urine output
• Metabolic acidosis
• Tachypnea
• Weak central pulses

Signs of decompensated shock include the signs listed above plus hypotension. In the absence of blood pressure measurement, decompensated shock is indicated by the nondetectable distal pulses with weak central pulses in an infant or child with other signs and symptoms consistent with inadequate tissue oxygen delivery.

The most common cause of shock is hypovolemia, one form of which is hemorrhagic shock. Distributive and cardiogenic shock are seen less often.

Learn to integrate the signs of shock because no single sign confirms the diagnosis. For example:
• Capillary refill time alone is not a good indicator of circulatory volume, but a capillary refill time of >2 seconds is a useful indicator of moderate dehydration when combined with a decreased urine output, absent tears, dry mucous membranes, and a generally ill appearanc. It is influenced by ambient temperature, lighting, site, and age.
• Tachycardia also results from other causes (eg, pain, anxiety, fever).
• Pulses may be bounding in anaphylactic, neurogenic, and septic shock.

In compensated shock, blood pressure remains normal; it is low in decompensated shock. Hypotension is a systolic blood pressure less than the 5th percentile of normal for age, namely:
• <60 mm Hg in term neonates (0 to 28 days)
• <70 mm Hg in infants (1 month to 12 months)
• <70 mm Hg + (2 x age in years) in children 1 to 10 years
• <90 mm Hg in children 10 years of age

Airway

Oropharyngeal and Nasopharyngeal Airways
Oropharyngeal and nasopharyngeal airways are adjuncts for maintaining an open airway. Oropharyngeal airways are used in unconscious victims (ie, with no gag reflex). Select the correct size: an oropharyngeal airway that is too small will not keep the tongue from obstructing the pharynx; one that is too large may obstruct the airway.

Nasopharyngeal airways will be better tolerated than oral airways by patients who are not deeply unconscious. Small nasopharyngeal tubes (for infants) may be easily obstructed by secretions.

Laryngeal Mask Airway
When endotracheal intubation is not possible, the LMA is an acceptable adjunct for experienced providers, but it is associated with a higher incidence of complications in young children.

Breathing: Oxygenation and Assisted Ventilation

Oxygen
Use 100% oxygen during resuscitation (Class Indeterminate). Monitor the patient’s oxygen level. When the patient is stable, wean the supplementary oxygen if the oxygen saturation is maintained.

Pulse Oximetry
If the patient has a perfusing rhythm, monitor oxygen saturation continuously with a pulse oximeter because clinical recognition of hypoxemia is not reliable. Pulse oximetry, however, may be unreliable in a patient with poor peripheral perfusion.

Bag-Mask Ventilation
Bag-mask ventilation can be as effective as ventilation through an endotracheal tube for short periods and may be safer.

Precautions
Victims of cardiac arrest are frequently overventilated during resuscitation. Excessive ventilation increases intrathoracic pressure and impedes venous return, reducing cardiac output, cerebral blood flow, and coronary perfusion. Excessive ventilation also causes air trapping and barotrauma in patients with small-airway obstruction and increases the risk of stomach inflation, regurgitation, and aspiration.

Minute ventilation is determined by the tidal volume and ventilation rate. Use only the force and tidal volume needed to make the chest rise visibly. During CPR for the patient with no advanced airway (eg, endotracheal tube, esophageal-tracheal combitube [Combitube], LMA) in place, ventilation rate is determined by the compression-ventilation ratio. Pause after 30 compressions (1 rescuer) or after 15 compressions (2 rescuers) to give 2 ventilations with mouth-to-mouth, mouth-to-mask, or bag-mask techniques. Give each breath over 1 second.

If an advanced airway is in place during CPR (eg, endotracheal tube, Combitube, LMA), ventilate at a rate of 8 to 10 times per minute without pausing chest compressions. In the victim with a perfusing rhythm but absent or inadequate respiratory effort, give 12 to 20 breaths per minute. One way to achieve this rate with a ventilating bag is to use the mnemonic "squeeze-release-release" at a normal speaking rate.

Gastric Inflation
Gastric inflation may interfere with effective ventilation and cause regurgitation. You can minimize gastric inflation by doing the following:
• Avoid excessive peak inspiratory pressures (eg, by ventilating slowly and watching chest rise). To avoid use of excessive volume, deliver only the volume needed to produce visible chest rise.
• Apply cricoid pressure. You should do so only in an unresponsive victim. This technique may require an additional (third) rescuer if the cricoid pressure cannot be applied by the rescuer who is securing the bag to the face. Avoid excessive pressure so as not to obstruct the trachea.
• If you intubate the patient, pass a nasogastric or orogastric tube after you intubate because a gastric tube interferes with the gastroesophageal sphincter, allowing possible regurgitation.

Rapid Sequence Intubation
To facilitate emergency intubation and reduce the incidence of complications, skilled, experienced providers may use sedatives, neuromuscular blocking agents, and other medications to rapidly sedate and paralyze the victim. Use RSI only if you are trained and have experience using these medications and are proficient in the evaluation and management of the pediatric airway. If you use RSI you must have a secondary plan to manage the airway in the event that you cannot achieve intubation.

Cuffed Versus Uncuffed Tubes
In the in-hospital setting a cuffed endotracheal tube is as safe as an uncuffed tube for infants beyond the newborn period and in children. In certain circumstances (eg, poor lung compliance, high airway resistance, or a large glottic air leak) a cuffed tube may be preferable provided that attention is paid to endotracheal tube size, position, and cuff inflation pressure. Keep cuff inflation pressure <20 cm H2O.

Endotracheal Tube Size
Uncuffed endotracheal tube size (mm ID) =(age in years/4) + 4 The formula for estimation of a cuffed endotracheal tube size is as follows: Cuffed endotracheal tube size (mm ID) = (age in years/4) + 3 Endotracheal tube size, however, is more reliably based on a child’s body length. Length-based resuscitation tapes are helpful for children up to approximately 35 kg.

Verification of Endotracheal Tube Placement
Look for bilateral chest movement and listen for equal breath sounds over both lung fields, especially over the axillae.
• Listen for gastric insufflation sounds over the stomach (they should not be present if the tube is in the trachea).
• Use a device to evaluate placement. Check for exhaled CO2 (see below) if there is a perfusing rhythm. If the child has a perfusing rhythm and is >20 kg, you may use an esophageal detector device to check for evidence of esophageal placement (see below).
• Check oxygen saturation with a pulse oximeter. Following hyperoxygenation, the oxyhemoglobin saturation detected by pulse oximetry may not demonstrate a fall indicative of incorrect endotracheal tube position (ie, tube misplacement or displacement) for as long as 3 minutes.
• If you are still uncertain, perform direct laryngoscopy and look to see if the tube goes between the cords.
• In hospital settings perform a chest x-ray to verify that the tube is not in the right main bronchus and to identify a high tube position at risk of easy displacement.

After you secure the tube, maintain the patient’s head in a neutral position; neck flexion pushes the tube farther into the airway, and extension pulls the tube out of the airway.

If an intubated patient’s condition deteriorates, consider the following possibilities (DOPE):
• Displacement of the tube from the trachea
• Obstruction of the tube
• Pneumothorax
• Equipment failure

Exhaled or End-Tidal CO2 Monitoring
In infants and children with a perfusing rhythm, use a colorimetric detector or capnography to detect exhaled CO2 to confirm endotracheal tube position. A color change or the presence of a capnography waveform confirms tube position in the trachea but does not rule out right main bronchus intubation. During cardiac arrest, if exhaled CO2 is not detected, confirm tube position with direct laryngoscopy because the absence of CO2 may be a reflection of low pulmonary blood flow.

You may also detect a low end-tidal CO2 in the following circumstances:
• If the detector is contaminated with gastric contents or acidic drugs (eg, endotracheally administered epinephrine), you may see a constant color rather than breath-to-breath color change.
• An intravenous (IV) bolus of epinephrine may transiently reduce pulmonary blood flow and exhaled CO2 below the limits of detection.
• Severe airway obstruction (eg, status asthmaticus) and pulmonary edema may impair CO2 elimination.

Circulation

Advanced cardiovascular life support techniques are useless without effective circulation, which is supported by good chest compressions during cardiac arrest. Good chest compressions require an adequate compression rate (100 compressions per minute), an adequate compression depth (about one third to one half of the anterior-posterior diameter), full recoil of the chest after each compression, and minimal interruptions in compressions. Unfortunately, good compressions are not always performed for many reasons, including rescuer fatigue and long or frequent interruptions to secure the airway, check the heart rhythm, and move the patient.

Backboard
A firm surface that extends from the shoulders to the waist and across the full width of the bed provides optimal support for effective chest compressions. In ambulances and mobile life support units, use a spine board.

CPR Techniques and Adjuncts
There is insufficient data to make a recommendation for or against the use of mechanical devices to compress the sternum, active compression-decompression CPR, interposed abdominal compression CPR, pneumatic antishock garment during resuscitation from cardiac arrest, and open-chest direct heart compession.

Extracorporeal Membrane Oxygenation
Consider extracorporeal CPR for in-hospital cardiac arrest refractory to initial resuscitation attempts if the condition leading to cardiac arrest is reversible or amenable to heart transplantation, if excellent conventional CPR has been performed after no more than several minutes of no-flow cardiac arrest (arrest time without CPR), and if the institution is able to rapidly perform extracorporeal membrane oxygenation. Long-term survival is possible even after >50 minutes of CPR in selected patients.

Cardiovascular Monitoring
Attach electrocardiographic (ECG) monitoring leads or defibrillator pads as soon as possible and monitor blood pressure. If the patient has an indwelling arterial catheter, use the waveform to guide your technique in compressing the chest. A minor adjustment of your hand position or depth of compression can significantly improve the waveform.

Vascular Access

Vascular access is essential for administering medications and drawing blood samples. Venous access can be challenging in infants and children during an emergency, whereas intraosseous (IO) access can be easily achieved. Limit the time you attempt venous access, and if you cannot achieve reliable access quickly, establish IO access. In cardiac arrest immediate IO access is recommended if no other IV access is already in place.

Intraosseous Access
IO access is a rapid, safe, and effective route for the administration of medications and fluids, and it may be used for obtaining an initial blood sample during resuscitation. You can safely administer epinephrine, adenosine, fluids, blood products, and catecholamines. Onset of action and drug levels achieved are comparable to venous administration. You can also obtain blood specimens for type and crossmatch and for chemical and blood gas analysis even during cardiac arrest, but acid-base analysis is inaccurate after sodium bicarbonate administration via the IO cannula. Use manual pressure or an infusion pump to administer viscous drugs or rapid fluid boluses, and follow each medication with a saline flush to promote entry into the central circulation.

Venous Access
A central intravenous line (IV) provides more secure long-term access, but central drug administration does not achieve higher drug levels or a substantially more rapid response than peripheral administration.

Endotracheal Drug Administration
If you cannot establish vascular access, you can give lipid-soluble drugs such as lidocaine, epinephrine, atropine, and naloxone ("LEAN") via the endotracheal tube, although optimal endotracheal doses are unknown. Flush with a minimum of 5 mL normal saline followed by 5 assisted manual ventilations. If CPR is in progress, stop chest compressions briefly during administration of medications. Although naloxone and vasopressin may be given by the endotracheal route, there are no human studies to support a specific dose. Non–lipid-soluble drugs (eg, sodium bicarbonate and calcium) may injure the airway and should not be administered via the endotracheal route.

Administration of resuscitation drugs into the trachea results in lower blood concentrations than the same dose given intravascularly. Furthermore, recent animal studies suggest that the lower epinephrine concentrations achieved when the drug is delivered by the endotracheal route may produce transient ß-adrenergic effects. These effects can be detrimental, causing hypotension, lower coronary artery perfusion pressure and flow, and reduced potential for return of spontaneous circulation. Thus, although endotracheal administration of some resuscitation drugs is possible, IV or IO drug administration is preferred because it will provide a more predictable drug delivery and pharmacologic effect.

Emergency Fluids and Medications

Fluids
Use an isotonic crystalloid solution (eg, lactated Ringer’s solution or normal saline) to treat shock; there is no benefit in using colloid (eg, albumin) during initial resuscitation. Use bolus therapy with a glucose-containing solution to only treat documented hypoglycemia. There is insufficient data to make a recommendation for or against hypertonic saline for shock associated with head injuries or hypovolemia.

Medications

Adenosine
Adenosine causes a temporary atrioventricular (AV) nodal conduction block and interrupts reentry circuits that involve the AV node. It has a wide safety margin because of its short half-life.

Amiodarone
Amiodarone slows AV conduction, prolongs the AV refractory period and QT interval, and slows ventricular conduction (widens the QRS).

Precautions
Monitor blood pressure and administer as slowly as the patient’s clinical condition allows; it should be administered slowly to a patient with a pulse but may be given rapidly to a patient with cardiac arrest or ventricular fibrillation (VF). Amiodarone causes hypotension through its vasodilatory property. The severity of the hypotension is related to the infusion rate and is less common with the aqueous form of amiodarone.91

Monitor the ECG because complications may include bradycardia, heart block, and torsades de pointes ventricular tachycardia (VT). Use extreme caution when administering with another drug causing QT prolongation, such as procainamide. Consider obtaining expert consultation. Adverse effects may be long lasting because the half-life is up to 40 days.92

Atropine
Atropine sulfate is a parasympatholytic drug that accelerates sinus or atrial pacemakers and increases AV conduction.

Precautions
Small doses of atropine (<0.1 mg) may produce paradoxical bradycardia.93 Larger than recommended doses may be required in special circumstances (eg, organophosphate poisoning94 or exposure to nerve gas agents).

Calcium
Routine administration of calcium does not improve outcome of cardiac arrest.95 In critically ill children, calcium chloride may provide greater bioavailability than calcium gluconate.96 Preferably administer calcium chloride via a central venous catheter because of the risk of sclerosis or infiltration with a peripheral venous line.

Epinephrine
The -adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and thus coronary perfusion pressure, a critical determinant of successful resuscitation.97,98

Precautions
Administer all catecholamines through a secure line, preferably into the central circulation; local ischemia, tissue injury, and ulceration may result from tissue infiltration.

Do not mix catecholamines with sodium bicarbonate; alkaline solutions inactivate them. In patients with a perfusing rhythm, epinephrine causes tachycardia and may cause ventricular ectopy, tachyarrhythmias, hypertension, and vasoconstriction.99

Glucose
Infants have high glucose requirements and low glycogen stores and develop hypoglycemia when energy requirements rise.100 Check blood glucose concentrations during and after arrest and treat hypoglycemia promptly.

Lidocaine
Lidocaine decreases automaticity and suppresses ventricular arrhythmias102 but is not as effective as amiodarone for improving intermediate outcomes (ie, return of spontaneous circulation or survival to hospital admission) among adult patients with VF refractory to a shock and epinephrine.103 Neither lidocaine nor amiodarone has been shown to improve survival to hospital discharge among patients with VF cardiac arrest.

Precautions
Lidocaine toxicity includes myocardial and circulatory depression, drowsiness, disorientation, muscle twitching, and seizures, especially in patients with poor cardiac output and hepatic or renal failure.104,105

Magnesium
There is insufficient evidence to recommend for or against the routine administration of magnesium during cardiac arrest. Magnesium is indicated for the treatment of documented hypomagnesemia or for torsades de pointes (polymorphic VT associated with long QT interval). Magnesium produces vasodilation and may cause hypotension if administered rapidly.

Procainamide
Procainamide prolongs the refractory period of the atria and ventricles and depresses conduction velocity.

Precautions
There is little clinical data on using procainamide in infants and children.109,110 Infuse procainamide very slowly while you monitor for hypotension, prolongation of the QT interval, and heart block. Stop the infusion if the QRS widens to >50% of baseline or if hypotension develops. Use extreme caution when administering with another drug causing QT prolongation, such as amiodarone. Consider obtaining expert consultation.

Sodium Bicarbonate
The routine administration of sodium bicarbonate has not been shown to improve outcome of resuscitation. After you have provided effective ventilation and chest compressions and administered epinephrine, you may consider sodium bicarbonate for prolonged cardiac arrest. Sodium bicarbonate administration may be used for treatment of some toxidromes or special resuscitation situations. During cardiac arrest or severe shock, arterial blood gas analysis may not accurately reflect tissue and venous acidosis.

Precautions
Excessive sodium bicarbonate may impair tissue oxygen delivery113; cause hypokalemia, hypocalcemia, hypernatremia, and hyperosmolality114,115; decrease the VF threshold116; and impair cardiac function.

Vasopressin
There is limited experience with the use of vasopressin in pediatric patients,117 and the results of its use in the treatment of adults with VF cardiac arrest have been inconsistent.118–121 There is insufficient evidence to make a recommendation for or against the routine use of vasopressin during cardiac arrest.

Torsades de Pointes
This polymorphic VT is seen in patients with a long QT interval, which may be congenital or may result from toxicity with type IA antiarrhythmics (eg, procainamide, quinidine, and disopyramide) or type III antiarrhythmics (eg, sotalol and amiodarone), tricyclic antidepressants (see below), digitalis, or drug interactions.155,156 These are examples of contributing factors listed in the green box in the algorithm.

Treatment
Regardless of the cause, treat torsades de pointes with a rapid (over several minutes) IV

Special Resuscitation Situations

Trauma
Some aspects of trauma resuscitation require emphasis because improperly performed resuscitation is a major cause of preventable pediatric death.174 Common errors in pediatric trauma resuscitation include failure to open and maintain the airway, failure to provide appropriate fluid resuscitation, and failure to recognize and treat internal bleeding. Involve a qualified surgeon early, and if possible, transport a child with multisystem trauma to a trauma center with pediatric expertise.

The following are special aspects of trauma resuscitation:
• When the mechanism of injury is compatible with spinal injury, restrict motion of the cervical spine and avoid traction or movement of the head and neck. Open and maintain the airway with a jaw thrust, and do not tilt the head.
If you cannot open the airway with a jaw thrust, use head tilt–chin lift, because you must establish a patent airway. Because of the disproportionately large head size in infants and young children, optimal positioning may require recessing the occiput60 or elevating the torso to avoid undesirable backboard-induced cervical flexion.
• Do not overventilate even in case of head injury.176 Intentional brief hyperventilation may be used as a temporizing rescue therapy when you observe signs of impending brain herniation (eg, sudden rise in measured intracranial pressure, dilated pupil[s] not responsive to light, bradycardia, hypertension).
• Suspect thoracic injury in all thoracoabdominal trauma, even in the absence of external injuries. Tension pneumothorax, hemothorax, or pulmonary contusion may impair breathing.
• If the patient has maxillofacial trauma or if you suspect a basilar skull fracture, insert an orogastric rather than a nasogastric tube.
• Treat signs of shock with a bolus of 20 mL/kg of an isotonic crystalloid (eg, normal saline or lactated Ringer’s solution) even if blood pressure is normal. Give additional boluses (20 mL/kg) if systemic perfusion fails to improve. If signs of shock persist after administration of 40 to 60 mL/kg of isotonic crystalloid, give 10 to 15 mL/kg of blood. Although type-specific crossmatched blood is preferred, in an emergency use O-negative blood in females and O-positive or O-negative in males. If possible warm the blood before rapid infusion.
• Consider intra-abdominal hemorrhage, tension pneumothorax, pericardial tamponade, spinal cord injury in infants and children, and intracranial hemorrhage in infants with signs of shock.

Toxicologic Emergencies
Overdose with cocaine, narcotics, tricyclic antidepressants, calcium channel blockers, and ß-adrenergic blockers poses some unique resuscitation problems in addition to the usual resuscitative measures.

Cocaine
Acute coronary syndrome, manifested by chest pain and cardiac rhythm disturbances (including VT and VF), is the most frequent cocaine-related reason for hospitalization in adults. Cocaine prolongs the action potential and QRS duration and impairs myocardial contractility.

Treatment
• Cool aggressively; hyperthermia is associated with an increase in toxicity.
• For coronary vasospasm, consider nitroglycerin, a benzodiazepine, and phentolamine.
• Do not give ß-adrenergic blockers.
• For ventricular arrhythmia, consider sodium bicarbonate (1 to 2 mEq/kg) in addition to standard treatments.
• To prevent arrhythmia secondary to myocardial infarction, consider a lidocaine bolus followed by a lidocaine infusion.

Tricyclic Antidepressants and Other Sodium Channel Blockers Toxic doses cause cardiovascular abnormalities, including intraventricular conduction delays, heart block, bradycardia, prolongation of the QT interval, ventricular arrhythmias (including torsades de pointes, VT, and VF), hypotension,189,197 seizures, and a depressed level of consciousness.

Treatment
• Give 1 to 2 mEq/kg boluses of sodium bicarbonate until arterial pH is >7.45, and then infuse 150 mEq NaHCO3 per liter of D5W to maintain alkalosis. In severe intoxication, increase the pH to 7.50 to 7.55. Do not administer Class IA (quinidine, procainamide), Class IC (flecainide, propafenone), or Class III (amiodarone and sotalol) antiarrhythmics, which may exacerbate cardiac toxicity.
• For hypotension, give boluses (10 mL/kg each) of normal saline. If you need a vasopressor, epinephrine and norepinephrine have been shown to be more effective than dopamine in raising blood pressure.
• Consider extracorporeal membrane oxygenation if high-dose vasopressors do not maintain blood pressure.

Calcium Channel Blockers
Manifestations of toxicity include hypotension, ECG changes (prolongation of the QT interval, widening of the QRS, and right bundle branch block), arrhythmias (bradycardia, SVT, VT, torsades de pointes, and VF),203 and altered mental status.

Treatment
• Treat mild hypotension with small boluses (5 to 10 mL/kg) of normal saline because myocardial depression may limit the amount of fluid the patient can tolerate.
• The effectiveness of calcium administration is variable. Try giving 20 mg/kg (0.2 mL/kg) of 10% calcium chloride over 5 to 10 minutes; if there is a beneficial effect, give an infusion of 20 to 50 mg/kg per hour. Monitor ionized calcium concentration to prevent hypercalcemia. It is preferable to administer calcium chloride via a central venous catheter; use caution when infusing into a peripheral IV because of the risk for sclerosis or infiltration.
• For bradycardia and hypotension, consider a high-dose vasopressor such as norepinephrine or epinephrine.
• There is insufficient data to recommend for or against an infusion of insulin and glucose208–211 or sodium bicarbonate.

ß-Adrenergic Blockers
Toxic doses of ß-adrenergic blockers cause bradycardia, heart block, and decreased cardiac contractility, and some (eg, propranolol and sotalol) may also prolong the QRS and the QT intervals.211–214

Treatment
• High-dose epinephrine infusion may be effective.
• Consider glucagon. In adolescents, infuse 5 to 10 mg of glucagon over several minutes followed by an IV infusion of 1 to 5 mg/h. If you are giving >2 mg of glucagon, reconstitute it in sterile water (<1 mg/mL) rather than the diluent supplied by the manufacturer.
• Consider an infusion of glucose and insulin
• There is insufficient data to make a recommendation for or against using calcium. Calcium may be considered if glucagon and catecholamine are ineffective.

Opioids
Narcotics may cause hypoventilation, apnea, bradycardia, and hypotension.

Treatment
• Ventilation is the initial treatment for severe respiratory depression from any cause.
• Naloxone reverses the respiratory depression of narcotic overdose, but in persons with long-term addictions or those with cardiovascular disease, naloxone may increase heart rate and blood pressure and cause acute pulmonary edema, cardiac arrhythmias (including asystole), and seizures. Ventilation before administration of naloxone appears to reduce these adverse effects.225 Intramuscular administration of naloxone may lower the risk.

Postresuscitation Stabilization
The goals of postresuscitation care are to preserve brain function, avoid secondary organ injury, diagnose and treat the cause of illness, and enable the patient to arrive at a pediatric tertiary-care facility in an optimal physiological state. Reassess frequently because cardiorespiratory status may deteriorate.

Respiratory System
Continue supplementary oxygen until you confirm adequate blood oxygenation and oxygen delivery. Monitor by continuous pulse oximetry.

Intubate and mechanically ventilate the patient if there is significant respiratory compromise (tachypnea, respiratory distress with agitation or decreased responsiveness, poor air exchange, cyanosis, hypoxemia). If the patient is already intubated, verify tube position, patency, and security. In the hospital setting, obtain arterial blood gases 10 to 15 minutes after establishing the initial ventilatory settings and make appropriate adjustments. Ideally correlate blood gases with capnographic end-tidal CO2 concentration to enable noninvasive monitoring of ventilation.

Control pain and discomfort with analgesics (eg, fentanyl or morphine) and sedatives (eg, lorazepam, midazolam). In very agitated patients, neuromuscular blocking agents (eg, vecuronium or pancuronium) with analgesia or sedation, or both, may improve ventilation and minimize the risk of tube displacement. Neuromuscular blockers, however, will mask seizures.

Insert a gastric tube to relieve and help prevent gastric inflation.

Cardiovascular System

Continuously monitor heart rate, blood pressure (by direct arterial line if possible), and oxygen saturation. Repeat clinical evaluations at least every 5 minutes until the patient is stable. Monitor urine output with an indwelling catheter.

As a minimum, perform the following laboratory tests: central venous or arterial blood gas analysis and measurement of serum electrolytes, glucose, and calcium levels. A chest x-ray may help you evaluate endotracheal tube position, heart size, and pulmonary status.

Myocardial dysfunction is common after cardiac arrest.227,228 Systemic and pulmonary vascular resistance are increased except in some cases of septic shock.229 Vasoactive agents may improve hemodynamics, but each drug and dose must be tailored to the patient because clinical response is variable. Infuse all vasoactive drugs into a secure IV line. The potential adverse effects of catecholamines include local ischemia and ulceration, tachycardia, atrial and ventricular tachyarrhythmias, hypertension, and metabolic changes (hyperglycemia, increased lactate concentration,230 and hypokalemia).

Epinephrine
Low-dose infusions (<0.3 µg/kg per minute) generally produce ß-adrenergic action (potent inotropy and decreased systemic vascular resistance), and higher-dose infusions (>0.3 µg/kg per minute) cause -adrenergic vasoconstriction.231 Because there is great interpatient variability,232,233 titrate the drug to the desired effect. Epinephrine may be preferable to dopamine in patients (especially infants) with marked circulatory instability and decompensated shock.

Dopamine
Titrate dopamine to treat shock that is unresponsive to fluid and when systemic vascular resistance is low. Typically a dose of 2 to 20 µg/kg per minute is used. Although low-dose dopamine infusion has been frequently recommended to maintain renal blood flow or improve renal function, more recent data has failed to show a beneficial effect from such therapy. At higher doses (>5 µg/kg per minute), dopamine stimulates cardiac ß-adrenergic receptors, but this effect may be reduced in infants and in chronic congestive heart failure.231 Infusion rates >20 µg/kg per minute may result in excessive vasoconstriction.231

Dobutamine Hydrochloride
Dobutamine has a selective effect on ß1- and ß2-adrenergic receptors; it increases myocardial contractility and usually decreases peripheral vascular resistance. Titrate an infusion232,235,236 to improve cardiac output and blood pressure, especially due to poor myocardial function.236

Norepinephrine
Norepinephrine is a potent inotropic and peripheral vasoconstricting agent. Titrate an infusion to treat shock with low systemic vascular resistance (septic, anaphylactic, spinal, or vasodilatory) unresponsive to fluid.

Sodium Nitroprusside
Sodium nitroprusside increases cardiac output by decreasing vascular resistance (afterload). If hypotension is related to poor myocardial function, consider using a combination of sodium nitroprusside to reduce afterload and an inotrope to improve contractility.

Inodilators
Inodilators (inamrinone and milrinone) augment cardiac output with little effect on myocardial oxygen demand. Use an inodilator for treatment of myocardial dysfunction with increased systemic or pulmonary vascular resistance.237–239 Administration of fluids may be required because of the vasodilatory effects.

Inodilators have a long half-life with a long delay in reaching a new steady-state hemodynamic effect after changing the infusion rate (18 hours with inamrinone and 4.5 hours with milrinone). In case of toxicity, if you stop the infusion the adverse effects may persist for several hours.

Neurologic System
One goal of resuscitation is to preserve brain function. Prevent secondary neuronal injury by adhering to the following precautions:

• Do not provide routine hyperventilation. Hyperventilation has no benefit and may impair neurologic outcome, most likely by adversely affecting cardiac output and cerebral perfusion.175 Intentional brief hyperventilation may be used as temporizing rescue therapy in response to signs of impending cerebral herniation (eg, sudden rise in measured intracranial pressure, dilated pupil[s] not responsive to light, bradycardia, hypertension).
• When patients remain comatose after resuscitation, consider cooling them to a temperature of 32°C to 34°C for 12 to 24 hours because cooling may aid brain recovery. Prevent shivering by providing sedation and, if needed, neuromuscular blockade. Closely watch for signs of infection. Other complications of hypothermia include diminished cardiac output, arrhythmia, pancreatitis, coagulopathy, thrombocytopenia, hypophosphatemia, and hypomagnesemia. Neuromuscular blockade can mask seizures.
• Monitor temperature and treat fever aggressively with antipyretics and cooling devices because fever adversely influences recovery from ischemic brain injury.
• Treat postischemic seizures aggressively; search for a correctable metabolic cause such as hypoglycemia or electrolyte imbalance.

Renal System
Decreased urine output (<1 mL/kg per hour in infants and children or <30 mL/h in adolescents) may be caused by prerenal conditions (eg, dehydration, inadequate systemic perfusion), renal ischemic damage, or a combination of factors. Avoid nephrotoxic medications and adjust the dose of medications excreted by the kidneys until you have checked renal function.