Cardiopulmonary Resuscitation Overview
Cardiopulmonary arrest in infants and children is rarely a sudden event. The usual progression of arrest begins with hypoxia, hypercarbia, and acidosis resulting in respiratory failure, which eventually leads to asystolic cardiac arrest. Etiologies include sudden infant death syndrome (SIDS), respiratory disease, sepsis, major trauma, submersion, poisoning, metabolic/electrolyte imbalance, and congenital anomalies. In contrast, primary cardiac arrest is relatively rare in the pediatric age group and is most frequently caused by congenital heart disease, myocarditis, and chest trauma with myocardial injury. Although asystole and pulseless electrical activity (PEA) are the primary rhythms in pediatric cardiac arrest, patients with sudden cardiac arrest are likely to have ventricular tachycardia (VT) or ventricular fibrillation (VF).
The outcome of unwitnessed cardiopulmonary arrest in infants and children is poor. Less than 10% of pediatric patients who have out-of-hospital cardiac arrests survive to discharge and most are neurologically impaired. In contrast, about one-third of children with in-hospital cardiac arrest survive to hospital discharge, with a better neurological outcome.
Begin resuscitation with C-A-B: Chest compression, Airway and Breathing, as the key factor in return of spontaneous circulation (ROSC) and survival is the maintenance of adequate coronary artery and cerebral artery perfusion. This is best achieved by starting resuscitation with chest compressions. However, individualize the CPR sequence based upon the location of the arrest and the presumed etiology.
Emergency Department Priorities
To optimize outcome, it is essential to recognize early signs and symptoms of impending respiratory failure and circulatory shock prior to the development of full cardiopulmonary arrest. All equipment, supplies, and drugs must be available and organized for easy access. It is imperative that the staff have training in American Heart Association Pediatric Advanced Life Support (PALS), and routinely practice mock pediatric resuscitations. Pediatric Advanced Life Support utilizes a systematic approach to the assessment and treatment of seriously ill or injured pediatric patients.
In order to optimize care in a high-stress situation, use pre-calculated drug sheets or the Broselow tape, a height-based weight system for accurate dosing of resuscitation medication which also offers immediate access to pre-sized emergency equipment. In addition, develop and maintain a comprehensive plan to organize the resuscitation team (Figure 1.1). Assign a role to each team member: team leader, airway management, chest compressions, achieving vascular access, obtaining a history, medication administration, recorder, and runner. Identify a team leader early whose sole responsibility is to oversee the resuscitation and coordinate the team dynamics. Ideally, along with the physicians and nurses, a respiratory therapist and pharmacist will assist the team. Prepare the essential equipment needed for resuscitation in advance, using the mnemonic IMSOAPP (Table 1.1).
|I||IV fluids/IV catheter/intraosseous needle|
|M||Monitors: cardiorespiratory; pulse oximeter; blood pressure|
|S||Suction: tonsil tipped (Yankauer) and flexible catheters|
|O||100% Oxygen source|
|Bag-mask: different size masks|
|Oral airway: nasopharyngeal and oral|
|Laryngoscope with assorted blades: Miller, Macintosh|
|Tracheal tube: cuffed and uncuffed, multiple sizes|
|P||Pharmacy: medications, either a pre-calculated drug sheet or Broselow tape|
|P||Personnel: call a code, have resuscitation team available|
Rapid Cardiopulmonary Assessment
Quickly perform a primary evaluation, which focuses on the Appearance, Airway, Breathing and Circulatory (ABCs) status of the patient. This initial examination provides assessment of the patient’s acuity, and prioritizes the urgency and aggressiveness of intervention in response to the degree of physiologic compromise. Following stabilization of the ABCs, the secondary assessment includes a complete head-to-toe examination of the patient, while maintaining normothermia and normoglycemia.
Assess the general appearance of the patient. Evaluate the activity level of the child, reaction to painful or unfamiliar stimuli, interaction with the caretaker, consolability, and the strength of cry, relative to the patient’s age.
Airway patency is particularly prone to early compromise in pediatric patients, as the airway diameter and length are smaller than in adults. Determine whether the airway is clear (no intervention required), maintainable with noninvasive intervention (positioning, suctioning, oropharyngeal or nasopharyngeal airway placement, bag-mask ventilation) or not maintainable without intubation.
Ventilation and oxygenation are reflected in the work of breathing and can be quickly assessed by the mnemonic RACE:
Rate: age-dependent. Tachypnea is often the first sign of respiratory distress, but it may also be secondary to acidosis.
– listen to breath sounds in all areas: anterior and posterior chest, axillae
– a priority is to rule-out tension pneumothorax: absent breath sounds, tracheal deviation
– abnormal sounds: rales, rhonchi, wheezing.
– pink, pallid, cyanotic, or mottled
– pulse oximetry: use the O2 saturation as the fifth vital sign.
– “Tripod” position, nasal flaring, grunting, stridor, head bobbing;
– Accessory muscle use: sternocleidomastoid prominence;
– Retractions: suprasternal, subcostal, intercostal.
The presence of abnormal clinical signs of breathing such as grunting, severe retractions, mottled color, use of accessory muscles, and cyanosis are precursors to impending respiratory failure.
The circulatory status reflects the effectiveness of cardiac output as well as end-organ perfusion. The rapid assessment includes:
– heart rate: age-dependent
– central and peripheral pulses: compare the femoral, brachial, and radial pulses
– blood pressure: age-dependent; use the following guidelines to estimate the lowest acceptable (fifth percentile) systolic BP:
Newborn to 1 month = 60 mm Hg
1 month to 1 year = 70 mm Hg
1–10 years = 70 mm Hg + ( 2 × age in years)
>10 years = 90 mm Hg.
End-organ perfusion (systemic circulation):
– skin perfusion: capillary refill (<2 seconds normal), color, extremity temperature (relative to ambient temperature)
– renal perfusion: urinary output = 0.5–1 mL/kg/h (about 30 mL/h for an adolescent)
– CNS perfusion: mental status, level of consciousness, irritability, consolability, AVPU response:
responsive to voice
responsive to pain
Tachycardia and tachypnea are early signs of cardiorespiratory compromise. Observe for central or peripheral cyanosis and feel the skin temperature and moisture. With the fingers at the level of the heart, apply pressure to the nail bed until it blanches, then release, timing the interval until the fingertip “pinks up.” Delayed capillary refill (>2 seconds), and cool, clammy extremities are clinical indicators of poor perfusion. A systolic blood pressure below the fifth percentile (measured with an appropriate-size cuff), loss of central pulses, oliguria, and altered level of consciousness are ominous signs of impending hypotensive/decompensated circulatory shock.
Immediate goals in the emergency department (ED) include supporting ventilation and organ perfusion. After a quick initial assessment, determine if the child is responsive and is breathing with a pulse. If the patient is unresponsive, not breathing or only gasping, without a pulse, immediately start CPR starting with chest compression, open and maintain the airway, support ventilation and perfusion, and identify and treat reversible causes (Table 1.2 and Figure 1.2).
Airway management is always the initial priority. To open the airway, first use simple maneuvers such as repositioning the head, suctioning secretions from the mouth, and placing an oropharyngeal or nasopharyngeal airway.
Head Tilt–Chin Lift
Open the airway using the head tilt–chin lift technique or jaw thrust maneuver. In an unresponsive child, perform the head tilt–chin lift maneuver by placing one hand on the patient’s forehead and gently tilting the head back into a neutral position. Curl the fingers of the other hand gently under the jaw near the chin, and lift the mandible upward to open the airway.
In a known or suspected trauma victim, use the jaw thrust maneuver without head extension. Protect the cervical spine by providing manual in-line traction. Place one hand on each side of the patient’s head to hold it still, since immobilization devices may interfere with maintaining a patent airway. Perform the jaw thrust by keeping the head midline, placing the fingers at the angle of the jaw on both sides, and lifting the mandible upward and forward without extending the neck. If a jaw thrust does not open the airway, protect the C-spine and use a gentle head tilt–chin lift maneuver to open the airway, since maintaining airway patency is critical in providing adequate ventilation.
Suction secretions and blood from the nasal passages, oropharynx, and trachea with flexible suction catheters. These must be available in sizes small enough to pass through the smallest endotracheal tube (ETT). A 5 Fr catheter will pass through a 2.5 mm ETT (usually 2 × the ETT size). Large rigid tonsil tip catheters (Yankauer) have rounded tips which are less likely to injure the tonsils and are useful for clearing blood and particulate matter from the mouth and hypopharynx. Limit suctioning to less than ten seconds, while monitoring the pulse oximeter and heart rate, as vigorous suctioning may cause vagal stimulation resulting in bradycardia and hypoxia.
The oropharyngeal airway is an adjunct for ventilating an unresponsive patient with an absent gag reflex. It will keep the base of the tongue away from the posterior pharyngeal wall to maintain airway patency, and it will also serve as a bite block in intubated patients. Do not use in an awake patient as it can precipitate vomiting and laryngospasm.
An appropriately sized oral airway extends from the corner of the patient’s mouth to the angle of the jaw. Use a tongue depressor to push the tongue down, and insert the oropharyngeal airway with its curvature along the hard palate. In infants and children, avoid inserting an airway that is too large. Do not attempt to insert the airway in an inverted position and then rotate it 180°, as this technique may damage the palate and push the base of the tongue posteriorly, occluding the airway. The proximal part of the oral airway is firm and flat and is designed to be placed between the teeth to prevent biting (the tracheal tube or your finger). Tape the flange to the lips to prevent it from being dislodged.
Use a nasopharyngeal airway in an obtunded patient with an intact gag reflex to prevent upper airway obstruction secondary to a floppy tongue. Estimate the size by measuring the distance from the tip of the nose to the tragus of the ear; the appropriately sized airway extends from the nostril to the base of the tongue without compressing the epiglottis. Lubricate the device and gently insert it along the floor of the nostril to avoid injuring the nasal mucosa or adenoids. A nasopharyngeal airway is contraindicated in a patient with a suspected basilar skull or nasal bone fracture.
Foreign Body Airway Obstruction
If choking or airway obstruction from a foreign body is suspected and the patient is awake and can speak, make no attempts to remove the object. Allow the patient to cough and clear the airway while observing for signs of complete obstruction (i.e., the victim is gagging, struggling to breathe, has high-pitched noise while breathing, is unable to make a sound, or is cyanotic). Remove the foreign body from the mouth only if it is visible. Do not perform blind finger sweeps in any age because the obstructing object may be pushed further into the pharynx and cause complete airway obstruction. If the patient deteriorates, use the following procedures, as summarized in Table 1.2.
Infants <1 Year of Age
Lay the infant prone over your thighs, with the head supported in a dependent position. Alternatively, hold the infant over your arm, in the prone position, supporting the head in your hand. Deliver five sharp back slaps, in rapid succession, between the baby’s scapulae. Turn the infant over and give five chest thrusts using two fingers on the mid-sternum, as in giving chest compressions. Look into the mouth to see if the foreign body is dislodged. Repeat these maneuvers until the object is expelled or the infant becomes unconscious. Do not perform abdominal thrusts in infants as there is risk of injury to the abdominal organs.
First open the mouth wide by grasping the tongue and jaw, and look for the foreign body in the oral cavity. If an object is seen, remove it, but do not perform a blind finger sweep. If there is no improvement, begin cardiopulmonary resuscitation (CPR) providing five cycles (30 compressions and 2 breaths per cycle) over 2 min. If breaths cannot be delivered, reposition the head and try again, or proceed with advanced airway maneuvers until respirations have been restored.
Children >1 Year of Age to Adolescent
Use the Heimlich abdominal thrust maneuver in this age group. If the patient is awake, stand or kneel behind the child and position the heel of the hand in the midline of the epigastrium with the other hand on top of the first, then give a rapid series of separate and distinct upward thrusts. With each thrust use sufficient force to dislodge the foreign body. For a small child, the heel of one hand is sufficient, as overly vigorous abdominal thrusts may cause damage to internal organs. If the patient loses consciousness, lay the child supine on the floor, reposition the head, and attempt to visualize the object. Do not attempt a blind finger sweep. If the object is not visualized, begin CPR, providing five cycles for 2 min.
A foreign body may also be removed under direct visualization with a laryngoscope and Magill forceps. Consult an otolaryngologist to remove more distal tracheal or laryngeal foreign bodies via flexible bronchoscopy.
Oxygenation, Ventilation, and Intubation
Once the airway has been stabilized and the breathing assessed, the need for oxygenation and ventilation takes priority. Provide supplemental oxygen to all patients with respiratory distress. Reassess breathing effort by physical examination and pulse oximetry. The equipment for airway support is described below.
Oxygen can be delivered by a low-flow or high-flow system. The actual oxygen concentration delivered by nasal cannula is unpredictable, so this method is appropriate only for a patient who requires minimal O2 supplementation. Low-flow oxygen is delivered by nasal cannula at rates of 1–4 L/min and provides O2 concentrations of 22–60%. However, flow rates >3 L/min are usually poorly tolerated by children, while flow rates >1–2 L/min may inadvertently administer positive pressure to newborns.
High-flow nasal cannula (HFNC) delivers an oxygen concentration of >60% at flow rates from 1–8 L/min in infants to 50–60 L/min in children and adults. Titrate the flow for additional inspiratory and expiratory pressure based on the patient’s work of breathing. High-flow nasal cannula uses a special device that warms and humidifies high flows of a combination of room air and oxygen. It can be used as an alternative to standard oxygen therapy or noninvasive positive pressure ventilation in a patient with acute hypoxemic respiratory distress without hypercapnia. Maximum deliverable flow rates vary by device manufacturer.
Simple O2 Mask
This is the most frequently used method for oxygen delivery in spontaneously breathing patients and it is more easily tolerated than nasal cannula. The actual O2 concentration that the patient receives is dependent on the flow rate and the patient’s ventilatory pattern, as room air enters through the ventilation holes on the sides of the mask. Oxygen flow rates of 6–10 L/min will deliver O2 concentrations of 35-60% and prevent rebreathing of exhaled CO2.
O2 Mask With Reservoir
A nonrebreather (NRB) mask is another form of high-flow delivery system which consists of a simple mask attached to a reservoir bag that is connected to an oxygen source. The NRB contains one-way valves at the exhalation ports to prevent the entrainment of room air, and a second valve at the reservoir bag to prevent the entry of exhaled gas back into the reservoir bag. The reservoir bag must be larger than the patient’s tidal volume (5–7 mL/kg) and remain inflated during inspiration. Oxygen concentrations up to 60% can be achieved in partial rebreathing systems, and >95% is possible if the oxygen flow rate is 10–15 L/min, and a good seal is maintained around the facemask.
For patients with respiratory failure, ventilate with a bag-mask apparatus until all the appropriate equipment and personnel for intubation are assembled. For optimum airway alignment, position the patient so that the auditory meatus is in line with the top of the anterior shoulder. Use the “sniffing” position in an older child by placing a folded towel under the head and elevating it. Due to a relatively larger head in an infant, keep the head midline and neck slightly extended with a pad under the shoulder. Flexing or overextending the neck may inadvertently obstruct the airway.
Adequate ventilation results in symmetric movement of the chest wall, with good breath sounds heard on auscultation. If the patient is making any respiratory effort, synchronize the delivered breaths with his or her efforts.
The most common system used to ventilate an apneic patient consists of a self-inflating bag (Ambu Bag), an O2 reservoir (corrugated tubing), and mask with a valve. These bags do not need a constant flow of O2 to refill. Using a reservoir with a supplemental oxygen flow rate of 10–15 L/min delivers 60–95% oxygen to the patient. Ensure that the corrugated tubing is pulled out to its full length to allow for the largest reservoir. If the bag has a pop-off valve set at 35–45 cm H2O, there must be a way to override it, since ventilatory pressure may be inadequate in patients with increased airway resistance or poor lung compliance.
Adequate ventilation requires an appropriate-size facemask, one that extends from the bridge of the nose to the cleft of the chin. The minimum volume for the bag in newborns, infants, and small children is 450–500 mL; use an adult bag (1000 mL or larger) for adolescents. If the only bags available are larger than the recommended size, ventilate infants and children by using the larger bag with a proper-size face mask and administering only enough volume to cause the chest to rise.
Use the E-C clamp technique to achieve proper ventilation with a bag-mask device. Hold the mask snugly to the face with the left thumb and index finger forming a “C.” Apply downward pressure over the mask to achieve a good seal, while avoiding pressure to the eyes. Place the remaining three fingers of the left hand, which form an “E,” on the mandible to lift the jaw, avoiding compression of the soft tissues of the neck. Using two hands to maintain the mask against the face (double E-C), while having a second provider compress the bag, will provide better ventilation than having a single provider perform bag-valve-mask alone.
Use a rate of 12–20 breaths per minute for an infant or child (Figure 1.2) (approximately one breath every 3–5 seconds). Squeeze the bag gently and deliver the breath over one second. Observe the chest rise, listen for breath sounds, and monitor the O2 saturation. Bagging too rapidly or using excessive pressure causes inflation of the stomach and barotrauma to the airways. If ventilation is difficult or breath sounds are unequal, reposition the head, suction the airway, switch to two-person bag-mask ventilation, and consider foreign body aspiration or pneumothorax. An oral or nasopharyngeal airway may help to maintain a patent airway during bag-mask resuscitation, and if the patient is ventilated for more than a few minutes, place a nasogastric tube to decompress air from the stomach to minimize the risk of aspiration from vomiting.
Tracheal intubation is the best way to manage the airway during cardiopulmonary resuscitation. The indications for tracheal intubation include:
respiratory failure despite effective initial intervention
lack of airway protective reflexes (gag, cough)
complete airway obstruction unrelieved by foreign body airway obstruction maneuvers
CNS disorder (increased intracranial pressure, inadequate control of ventilation)
Before attempting intubation, ensure that all necessary supplies, medications, and personnel are available. All equipment must be available in various sizes along with spare laryngoscope handles, bulbs, and batteries. A Broselow tape, which accurately correlates weight with length (for patients <35 kg), gives precise sizes of airway equipment, as well as appropriate drug doses. “Straight blades” (Miller) are often easier to use than “curved blades” (Macintosh) in infants and young children. Estimate laryngoscope blade size by measuring the distance from the incisors to the angle of the mandible. If the patient is between sizes, use a blade that is larger and then pull back to visualize the cords. See Table 1.3 for the most popular age-appropriate blade sizes.
|Premature to newborn||Miller 00–0|
|One month to toddler||Miller 1|
|18 months to 8 years||Miller 2, Macintosh 2|
|≥8 years||Macintosh 3|
Estimate the tracheal tube size by matching the diameter of the endotracheal tube (ETT) to the width of the nail of the patient’s fifth finger or the diameter of the nares. Tracheal tube size for different age groups is listed in Table 1.4. Alternatively, use the following formulas, but always have available tracheal tubes 0.5 mm larger and smaller than the calculated size:
|Age||Uncuffed ETT||Cuffed ETT||Depth|
|Premature||2.5 mm||–||6–7 mm|
|1 month to 1 year||3.5–4.0 mm||3.0 mm||10–11 mm|
|Older||4 + (age in years/4)||3 + (age in years/4)||3 × ETT size|
Previously, cuffed tracheal tubes were indicated only in children >8 years of age. Now, low-pressure cuffed tracheal tubes may be used in all ages (except newborns), provided the cuff inflation pressure is kept <20 cm H2O.
Prepare the tracheal tube with a stylet tip placed 1 cm from the distal end of the tube and bent in a gradual anterior curve at the distal third. The tip and cuff of the tube may be lubricated with viscous lidocaine or a water-soluble gel for easy passage.
In an emergency situation, perform oral intubation, which is easier than nasal intubation. In general, use a straight Miller laryngoscope blade for pediatric intubations. Have a tonsil tipped suction (Yankauer) and an appropriately sized flexible suction catheter readily available. To intubate the patient, keep the head midline in the “sniffing” position. If cervical spine trauma is a concern, have an assistant maintain manual in-line stabilization during the intubation, avoiding traction or movement of the neck. Continuously monitor the heart rate and pulse oximeter throughout the procedure.
Place the thumb and index finger of the (gloved) right hand into the right side of the patient’s mouth. Place the index finger on the patient’s upper teeth and the thumb on the lower teeth, using the scissor technique to open the mouth as wide as possible. Hold the laryngoscope in the left hand and introduce the blade into the right edge of the mouth, sweeping the tongue toward the left and out of the line of vision. Position a straight blade under the epiglottis and place a curved blade into the vallecula. Lift by pulling the handle of the laryngoscope up and away at a 45° angle to the floor, in the direction of the long axis of the handle. If the blade is in too deep, slowly withdraw it until the glottis pops into view. Be careful not to tilt the handle or blade, which may risk breaking or damaging the teeth.
The routine use of cricoid pressure (Sellick maneuver) during tracheal intubation in cardiac arrest is not recommended, as it may not prevent aspiration, while potentially interfering with the delivery of positive pressure breaths.
Once the vocal cords are exposed, introduce the ETT from the right side of the mouth (not down the barrel of the blade). Advance the ETT until the cuff just passes beyond the vocal cords. Uncuffed tubes often have a mark at the distal end of the tube, which when placed at the level of the cords will position the distal tip in the mid-trachea. As an alternative, estimate the tube depth to be equal to 3 × ETT size. A proper-size ETT easily passes through the cords. If it meets resistance in the subglottic area, do not try to force it through. Rather, replace it with a smaller tube. Hold the tube securely against the upper teeth or gums and carefully withdraw the laryngoscope first, and then remove the stylet from the ETT. If the patient was intubated with a cuffed tube, inflate the cuff to a pressure of <20 cm H2O.
Verify proper tube placement by listening for equal breath sounds and observing symmetrical rise of the chest. Confirm the presence of exhaled CO2 from the tracheal tube with either a colorimetric CO2 detector or capnography, and use a pulse oximeter to monitor oxygen saturation. Colorimetric devices are inaccurate if the patient does not have a perfusing rhythm (even with appropriate chest compressions) or the patient weighs <2 kg. Use continuous quantitative waveform capnography (PetCO2) to confirm correct placement of the ETT and to monitor intubated patients throughout the periarrest period. If breath sounds are louder over the stomach than the chest, or if it is unclear that the tube is in the trachea, remove the tracheal tube and ventilate by bag-mask. An audible air leak is expected with an uncuffed tube, but if there is a large air leak or none at all, the tube size may be inadequate; replace with an appropriately sized ETT. Secure the ETT to the patient’s face with tape or use a tracheal tube holder. Obtain a chest radiograph to confirm that the tip of the tube is opposite T2 (one fingerbreadth above the carina). Be aware that neck extension or head movement brings the tube higher, while neck flexion pushes the ETT deeper.
If the patient deteriorates after endotracheal intubation, use the mnemonic DOPE to reassess: Displacement of the tube into the esophagus or down the right mainstem bronchus; Obstruction of the tube with blood, secretions or kinking; Pneumothorax with decreased breath sounds and chest expansion on the affected side and deviation of trachea to the opposite side; or Equipment malfunction. If the patient is on a ventilator, disconnect and either attempt to ventilate with a bag or replace the ETT.
The goals of rapid-sequence intubation (RSI) are to create ideal intubating conditions by attenuating airway reflexes while minimizing elevations of intracranial pressure and maintaining adequate blood pressure. Rapid-sequence intubation is indicated for patients who require emergent tracheal intubation but are at high risk for pulmonary aspiration of gastric contents. Medications to facilitate intubation are rarely needed for patients who are moribund or in cardiac arrest, or for newborns within a few hours of delivery.
Anticipate the possibility of an unsuccessful intubation and prepare for alternate airway techniques before initiating sedation. Also, expect a difficult intubation and request help for patients with significant facial trauma, restricted neck extension, or if the tip of the uvula is not visible when the mouth is opened. Do not use sedation or muscle relaxation if there is any concern that bag-mask ventilation will be inadequate.
NEVER sedate or paralyze a patient whom you may not be able to ventilate!
Rapid-sequence intubation involves the use of premedications to minimize adverse events; sedative/hypnotic agents with rapid onset and short duration of activity; and neuromuscular blocking agents, with the goal of gaining immediate control of the airway, all performed in rapid sequence. Calculate and prepare all of the medications before beginning RSI.
While preparing for RSI, have the patient breathe 100% oxygen via a nonrebreather face mask for at least 3 min. If the patient is apneic or has inadequate respiratory effort, deliver 4–5 breaths by bag-mask in 30 seconds, which establishes an oxygen reserve that will last up to 4 min in an infant and longer in older children and adolescents. Providing continuous oxygen via nasal cannula during intubation (apneic oxygenation) may allow for a longer interval for attempting intubation before the patient experiences oxygen desaturation. During the period of pre-oxygenation, determine the likelihood of a difficult intubation, establish intravenous access, place the patient on cardiac and pulse oximeter monitors, and assemble all necessary equipment and personnel for tracheal intubation.
History and Physical Examination
No single feature on physical examination accurately predicts a difficult intubation. Therefore, perform a detailed pre-sedation assessment, including the SAMPLE history and a focused physical examination. A SAMPLE history is:
Signs and symptoms
Allergy: allergy to drugs, latex, foods
Medications: current prescription and nonprescription drugs
Past medical history: significant past medical and surgical history including asthma or bronchospasm, neuromuscular disease, previous difficult intubation(s), micrognathia, poor neck mobility
Last meal time: last oral intake and type of food
Upper Airway Examination
Ask a cooperative patient to open the mouth as wide as possible, with the tongue fully protruded. The Mallampati airway class I and II (visible faucial pillars and uvula) indicates relatively easier airway management (Figure 1.3). Use the “3–3–2 rule,” which is a predictor of difficult intubation in adults. The patient should be able to place three fingers between the open incisors, three fingers from the mental tubercle of the mandible to the thyroid (two fingers in children, one finger in infants), and two fingers from the laryngeal prominence to the floor of the mouth.
If the patient cannot cooperate, gently open the mouth (if possible) and use a direct laryngoscope blade in the manner of a conventional tongue blade to assess the size of the tongue compared with that of the oropharynx. If this assessment reveals a large tongue to oropharynx ratio or it cannot be done, assume that direct laryngoscopy will be difficult.
Premedications, Sedative/Hypnotics and Paralytics (Table 1.5)
The choice of premedication drugs for RSI will depend on the clinical situation as well as individual experience of the provider with these agents. The patient may be given a premedication agent (e.g., atropine or lidocaine), then a short-acting sedative/analgesic (e.g., etomidate, thiopental, midazolam, ketamine, fentanyl, or propofol) followed immediately by a short-acting muscle relaxant (e.g., succinylcholine or rocuronium).
|Normotensive||Etomidate 0.3 mg/kg|
|or Midazolam 0.3 mg/kg|
|or Propofol 1.5–3 mg/kg|
|Mild hypotension/no head injury||Etomidate 0.3 mg/kg|
|or Ketamine 1–2 mg/kg|
|or Fentanyl 1–4 mcg/kg|
|Severe hypotension/no head injury||None|
|or Etomidate 0.2–0.3 mg/kg|
|or Fentanyl 1–2 mcg/kg|
|Head injury/no hypotension||Etomidate 0.3 mg/kg|
|Head injury with mild hypotension||Etomidate 0.3 mg/kg|
|or Midazolam 0.1–0.2 mg/kg|
|Status asthmaticus||Ketamine 1–2 mg/kg|
|Status epilepticus||Midazolam 0.1–0.3 mg/kg|
Atropine (0.02 mg/kg; No Minimum Dose When Used as a Premedication for Emergency Intubation). Atropine as a premedication to prevent bradycardia is not routinely indicated. However, it may be useful in specific emergency intubations: when drugs (e.g., succinylcholine or fentanyl) which cause bradycardia are used; when the patient is already bradycardic at the time of intubation; or when there is a need to dry excessive secretions, permitting easier airway visualization during intubation.
Lidocaine (1–1.5 mg/kg). Lidocaine will attenuate the hypertension, tachycardia, and gagging response which occur during manipulation of the airway during laryngoscopy, when given 1–3 min prior. It may be useful for patients with head injuries and suspected raised intracranial pressure.
Etomidate (0.3 mg/kg). Etomidate is a short-acting anesthetic that decreases intracranial pressure but has minimal hemodynamic effects. It is the drug of choice for RSI in most clinical situations. Do not use etomidate if there is evidence of septic shock, since even a single dose can cause adrenal suppression, which is associated with a higher mortality rate in children. Since etomidate has no analgesic properties, small doses of fentanyl (1–2 mcg/kg) may also be needed.
Midazolam (0.1–0.3 mg/kg). This rapid-acting benzodiazepine produces potent amnesia and sedation. At RSI doses, which are higher than that used in procedural sedation, side effects include respiratory and myocardial depression.
Ketamine (1–2 mg/kg). Ketamine is a short-acting dissociative anesthetic agent that causes rapid sedation, amnesia, and analgesia. Ketamine maintains blood pressure and increases intracranial blood flow, which makes it useful for hypovolemic patients. It is also beneficial in patients with status asthmaticus, in whom it has been shown to decrease bronchospasm. Side effects include ICP elevation, emergence phenomenon, laryngospasm, and excessive airway secretions. Its use is relatively contraindicated in patients with hypertension, head injury, and psychiatric disorders. Excessive airway secretions may be controlled by pretreatment with atropine, and emergence reaction may be attenuated with midazolam.
Fentanyl (1–4 mcg/kg). Fentanyl is a rapid-acting narcotic analgesic with minimal cardiovascular effects, but it may cause respiratory depression. A significant side effect is chest wall rigidity, which usually occurs with rapid injection or using higher doses (10 mcg/kg). The combined use of opioid medications with benzodiazepines or other drugs that depress the CNS increase the risk of serious adverse reactions, including respiratory failure.
Propofol (1.5–3 mg/kg). Propofol is an extremely rapid-acting non-barbiturate sedative-hypnotic agent with no analgesic properties that produces general anesthesia. The onset of effect is extremely rapid, with short duration of action, and is an excellent induction agent in hemodynamically stable patients. It decreases ICP and cerebral metabolism, but also causes bradycardia and significant decrease in mean arterial blood pressure. This hypotensive effect limits its use in trauma patients. A pre-induction fluid bolus with normal saline may minimize its hypotensive effect. It is contraindicated in patients with egg or soy allergies.
Neuromuscular blocking agents (NMBs) rapidly cause paralysis and relaxation of the airway muscles by blocking the neuromuscular junction. Their use has been shown to significantly improve success of tracheal intubation and reduce complications. Use an NMB agent for all intubations unless there are contraindications, or if a difficult airway is anticipated. In such cases, use light sedation only.
Succinylcholine (infants: 1–2 mg/kg; children and adolescents 1–1.5 mg/kg). This is the most rapid-onset and shortest-acting muscle relaxant available. It is widely used because of its fast onset of action (<1 minute) and recovery (within 5–10 minute). Pretreatment with atropine may prevent potential serious bradyarrhythmias and excessive bronchial secretions (especially in children). Succinylcholine may cause an acute rise in intracranial pressure. Contraindications to using succinylcholine include: patients with chronic myopathy; increased intracranial and intraocular pressure; rhabdomyolysis (burn and crush injuries); preexisting hyperkalemia; and history of malignant hyperthermia.
Rocuronium (0.9–1.2 mg/kg). Rocuronium is a nondepolarizing muscle relaxant with a rapid onset of action (30–60 seconds) and minimal hemodynamic side effects. Myasthenia gravis is the only specific contraindication for this class of NMB agents. Rocuronium produces intubating conditions similar to succinylcholine, but with a longer duration of action (45 minutes versus 5–10 minutes).
Once the ETT is secured and the position is radiographically confirmed, provide adequate sedation and analgesia, and continue muscle paralysis with a long-acting agent (vecuronium or rocuronium) if indicated. To reduce the risk of aspiration, insert a nasogastric tube as soon as possible to decompress the stomach, especially in infants and children. However, use an orogastric tube if a basilar skull fracture or nasal fracture is suspected.
Initial Mechanical Ventilator Settings
The two modes of mechanical ventilation for emergency ventilation in children are pressure-limited and volume-limited support. For newborns and infants <10 kg, pressure-limited ventilators are most often used, while volume-limited ventilators are indicated for older children. When using pressure-limited ventilators, start with peak inspiratory pressures (PIP) of 15–25 cm H2O for newborns and 20–25 cm H2O for infants <1year of age, with a positive end-expiratory pressure (PEEP) of 3–5 cm H2O. Set the respiratory rate appropriate for age (20–40/min). For volume control ventilation, begin with tidal volumes of 6–8 mL/kg. Set an initial PEEP of 5 cm H2O, unless contraindicated, with respiratory rates of 20–30/min in children, and 12–20/min in adolescents. For both types of ventilators, initially use 100% O2, an inspiratory time of 0.8–1 second, and the inhale/exhale (I/E) ratio set at 1:2. Once the initial settings have been established, monitor continuously, making appropriate adjustments as dictated by the patient’s clinical condition.
Alternate/Adjunctive Airway Techniques
Alternate advanced airway techniques are useful for securing a difficult airway when intubation is not feasible or unsuccessful. The presence of certain congenital anomalies (Pierre Robin, Beckwith–Wiedemann, Down syndrome), anatomical defects (neck mass, laryngeal hemangioma, subglottic stenosis), or disease states (epiglottitis, angioedema, facial/neck trauma) may necessitate the use of advanced airway techniques. These include HFNC, noninvasive positive pressure ventilation (NIPPV), Heliox, and laryngeal mask airways (LMA). Other advanced airway techniques, such as fiberoptic laryngoscopy, lighted stylet, needle cricothyrotomy, or surgical cricothyrotomy, require training and experience to perform successfully.
Noninvasive ventilation (NIV) provides short-term mechanical ventilation without placement of a tracheal tube in stable, spontaneously breathing, alert, and cooperative patients. Although tracheal intubation is often a life-saving procedure, NIV functions to bridge the gap between maximal medical management and intubation. Benefits include decreasing the work of breathing, improving oxygenation, and avoiding common complications of intubation. It is important to note that NIV is not a replacement for tracheal intubation in patients who have life-threatening respiratory failure or require airway protection. It is contraindicated in patients who are hemodynamically unstable, lethargic, vomiting, or have cardiac dysrhythmias. The decision to use NIV is dependent on the patient (conscious and cooperative), specific disease (status asthmaticus, bronchiolitis, acute pulmonary edema, and neuromuscular disease), and whether airway protection is required.
The common NIPPV methods include HFNC, continuous positive airway pressure (CPAP), and bilevel positive airway pressure (BiPAP). CPAP and BiPAP are delivered via a nasal or full-face mask in children and by nasal prongs in infants. Straps hold the BiPAP face mask firmly to the patient’s face to create a tight seal. Neonates, who are obligate nose breathers, generally do not tolerate BiPAP, but may benefit from nasal prong CPAP or HFNC. Typical initial settings for CPAP include an inspiratory positive airway pressure (IPAP) of 5 cm H2O, and for BiPAP 8–10 cm H2O, with an expiratory positive airway pressure (EPAP) of 5 cm H2O. Titrate these settings upwards in 2 cm H2O increments until the desired effects are achieved. Adjust the FiO2 to maintain a target oxygen saturation of >92–95%. Start HFNC at 1–2 L/kg/min, and titrate up based on patient response.
Monitor the patient closely for worsening respiratory failure with serial lung exams, vital signs and oxygen saturation measurements. If the patient’s respiratory status worsens or does not improve, discontinue NIPPV and perform tracheal intubation.
Helium is a biologically inert gas that decreases turbulent gas flow when mixed with oxygen. Heliox improves delivery of oxygen and aerosolized medications to constricted peripheral airways, thus reducing the work of breathing. It has been used in conditions that are refractory to medical measures, such as status asthmaticus, moderate to severe bronchiolitis, and severe croup. Heliox is delivered in mixtures of 80% helium and 20% oxygen (80/20 Heliox) or 70% helium and 30% oxygen (70/30 Heliox). The low FiO2 in the gas mixture is an important limitation of Heliox use, so that it may not be adequate to use for patients with hypoxemia. Administer to spontaneously breathing patients by using a facemask and reservoir bag. Improvement of oxygenation and reduction of respiratory distress generally occurs within several minutes of Heliox initiation. If there is no improvement, or worsening of the patient’s clinical status, change to an alternate method of ventilation.
Laryngeal Mask Airway
The laryngeal mask airway (LMA) is a supraglottic airway that is indicated for patients who require an airway but cannot be tracheally intubated or adequately ventilated with a bag-mask. It can be used in patients with decreased airway reflexes (i.e., obtunded or comatose). The LMA consists of a tube attached to a mask, rimmed with a soft, inflatable cuff. When properly placed, the LMA sits in the hypopharynx around the glottic opening and directs air into the trachea. Unlike a tracheal tube, it will not fully prevent aspiration of gastric contents into the trachea.
Select the appropriate-size LMA (Table 1.6) and check for possible air leaks by inflating the cuff. Hold the LMA like a pen, with the index finger of the dominant hand placed at the junction of the tube and proximal aspect of the mask. Lubricate the posterior surface of the deflated mask, and orient it so that the opening is directed toward the tongue. With one smooth motion, insert the mask firmly along the hard palate and advance until resistance is encountered. With the tip of the mask placed in the hypopharynx, inflate the cuff. Auscultate the lungs to confirm correct placement. If endotracheal intubation is subsequently necessary, insert the ETT blindly through the properly placed LMA as it will be directed into the trachea.
|Mask size||Patient size||Maximum cuff volume|
|1||Neonates/infants up to 5 kg||Up to 4 mL|
|1½||Infants 5–10 kg||Up to 7 mL|
|2||Infants/children 10–20 kg||Up to 10 mL|
|2½||Children 20–30 kg||Up to 14 mL|
|3||Children 30–50 kg||Up to 20 mL|
|4||Adults 50–70 kg||Up to 30 mL|
|5||Adults 70–100 kg||Up to 40 mL|
|6||Adults >100 kg||Up to 50 mL|
There are newer LMAs available for specific situations. One version (Proseal LMA) has a parallel drainage tube attached to the airway tube to allow passage of a nasogastric tube, potentially decreasing the risk of aspiration. Other variations include the intubating LMA (Fastrach LMA), which is designed to facilitate blind tracheal intubation while allowing for continuous positive pressure ventilation, and the LMA CTrach, which has a built-in fiberoptic video screen for ease of intubation.
After beginning chest compression and stabilization of ventilation, the next priority is establishing cardiovascular perfusion. However, in a real-life scenario, the code team, with assigned roles (Figure 1.1), will be performing all tasks simultaneously. Begin chest compressions in patients with cardiac arrest or in an unresponsive child with gasping respirations and a heart rate <60 bpm, associated with signs of poor perfusion (altered mental status, delayed capillary refill, thready or absent pulses, cool extremities, hypotension). To be effective, deliver chest compressions on a firm surface. Components of high-quality CPR include the following:
“Push fast.” Perform chest compressions at a rate of 100–120 compressions per minute. For the lone rescuer, use a compression–ventilation ratio of 30:2 for all ages. After giving 30 compressions, provide 2 breaths then immediately resume compressions, providing 5 cycles in about 2 minutes. For two-rescuer infant and child CPR, one provider performs 15 chest compressions while the second rescuer opens the airway with a head tilt–chin lift maneuver and delivers two breaths. A compression–ventilation ratio of 15:2 provides more ventilations per minute, which is appropriate for most hypoxic, hypercarbic pediatric arrests.
“Push hard.” For an infant, depress the chest at least one-third the anterior–posterior (AP) diameter of the chest, or approximately 1.5 inches (4 cm). For children and adolescents, depress the chest 2 inches (5 cm). Adequate compressions usually generate a pulse. Coordinate compressions with ventilations to avoid simultaneous delivery and minimize interruptions in chest compressions. However, once the airway is secured by tracheal intubation, compressions and ventilation may be asynchronous and still be effective.
Compression landmarks. In infants, the lone rescuer should compress the sternum with two fingers placed just below the intermammary line. Push straight down, making sure to make the compressions smooth, not jerky. Avoid compression over the xiphoid or ribs, which may damage internal organs. When CPR is provided by two rescuers, the two-thumb encircling hands technique is recommended. Place both the thumbs together over the lower third of the sternum and encircle the infant’s chest with both hands. Forcefully compress the sternum with the thumbs, being careful to not compress the lateral walls of the chest with the hands. In children, compress the lower half of the sternum with the heel of one or two hands. For adolescents, compress the lower half of the sternum with the heel of two hands. The long axis of both heels should be placed parallel with the long axis of the sternum; straighten the arms, lock the elbows, and position the shoulders over the arms so that the body weight is added to the force of the compressions.
Allow complete chest recoil. After each compression, allow the chest wall to recoil completely, which permits the heart to refill with blood and improves the blood flow to the body during CPR. Do not lean on the chest.
Minimize interruptions of chest compressions. Limit pulse check to under ten seconds. When chest compressions are interrupted, coronary perfusion pressure rapidly declines, which may require several chest compressions to restore adequate coronary pressure once compressions are resumed.
Rotate the compressor role approximately every two minutes, as rescuer fatigue is common and can lead to inadequate compression rate and depth, with deterioration in CPR quality. To prevent compressor fatigue, rescuers should switch compressor and ventilation roles approximately every five cycles (about two minutes). To minimize interruptions in chest compressions, the switch should be anticipated by the providers and accomplished as quickly as possible, ideally in under five seconds.
The level of end-tidal carbon dioxide tension (PetCO2) correlates with coronary and cerebral perfusion pressures and is predictive of the outcomes of cardiopulmonary resuscitation. The use of PetCO2 measurement may help guide therapy especially for monitoring cardiac output and the effectiveness of chest compressions during CPR or shock.
Spend no more than 1–2 minutes attempting peripheral vascular access in cardiac arrest or other emergent situations. Intraosseous access (IO) may be easily established and more rapidly achieved than IV access. In any patient requiring resuscitation, make sure to have two functioning lines.
The IO approach allows for rapid vascular access for patients of all ages. Any drug or fluid normally given through the IV route, including blood products, can be given via the IO needle, although high flow rates are not possible without using an infusion pump. The IO needle is an emergency access device only. Replace it with another secure intravascular catheter or central line as soon as possible to prevent complications, such as infection, or compartment syndrome from fluid extravasation.
The primary site for IO insertion is the proximal tibia. Other acceptable sites are the distal tibia, proximal humerus, and anterior superior iliac spine. Position the leg in external rotation, locate the tibial tuberosity, and palpate approximately two fingerbreadths (one fingerbreadth in infants) distally on the medial flat portion of the tibia. Prepare the puncture site with a topical antiseptic (e.g., povidone-iodine). In a conscious patient, anesthetize the puncture site with 1–2 mL of 1% lidocaine. Contraindications to IO needle placement include a fracture or overlying skin infection at the site.
The Jamshidi IO needle is available in 18 G for infants and 15 G for all others, while the Cook IO needle is available in 16 G and 18 G sizes. Select the appropriate site and direct the IO needle perpendicular to the bone. Puncture the skin first, so that the needle is touching the bone. For manual IO insertion, use steady pressure with a screwing motion until a sudden loss of resistance is felt, indicating that the needle has entered the marrow cavity. If placed correctly, the needle will stand freely and upright without support. Remove the stylet and aspirate with a syringe. Inability to aspirate blood does not indicate improper placement, while infusion of fluid easily without extravasation or resistance confirms proper placement. After proper placement is determined, tape the needle in place to prevent accidental dislodgement. If fluid does extravasate (the calf expands or feels cold), remove the needle and make an attempt on the other side. Do not attempt more than once in the same bone.
Shock and circulatory collapse may be the primary cause of cardiopulmonary arrest, and restoration of the circulating blood volume by fluid therapy is a mainstay of shock resuscitation. Once vascular access (peripheral IV, IO, central line) is established, give an initial fluid bolus of 20 mL/kg of an isotonic crystalloid solution. In patients who are critically ill or in cardiopulmonary arrest, use a syringe to infuse the fluid rapidly over a few minutes. If cardiogenic shock is suspected, give smaller fluid boluses of 5–10 mL/kg over 10–20 minutes and reassess after each bolus. For hypovolemic trauma victims, consider giving 10 mL/kg of O-negative packed red blood cells, if readily available.
Rapid infusion of dextrose-containing solutions results in an osmotic diuresis and is contraindicated in the initial phase of fluid resuscitation. Fluid resuscitation is particularly challenging in patients with cardiac disease, diabetic ketoacidosis (DKA), calcium channel or beta-blocker ingestion, or head injury, as restoring and maintaining adequate tissue perfusion must be balanced with the risk of worsening cardiac output or cerebral edema.
Base the decision to give additional IV fluids on frequent reassessments of perfusion: mental status, quality of pulses, blood pressure, heart rate, capillary refill, and urine output. In severe shock, give additional isotonic crystalloid solution boluses of 20 mL/kg, up to a total of 60 mL/kg, until the vital signs and perfusion are restored, while monitoring for signs of fluid overload. If further fluid is required, add pressors (see below) to increase myocardial contractility and maintain adequate vascular tone. If the patient is in septic shock, there may be significant capillary leakage. Large fluid volumes >60 mL/kg or 5% albumin given in 10 mL/kg doses may be required.
Vasoactive agents (Figure 1.4) are the drugs of choice for improving myocardial contractility and cardiac output in patients with shock who have received adequate fluid administration. Because of their short half-life and potency, they are given as an infusion. The choice of agent is determined by the etiology contributing to shock; they include epinephrine, norepinephrine, dopamine, dobutamine, milrinone, or inamrinone. In patients who remain hypotensive despite adequate fluid resuscitation, epinephrine infusion is preferable for children with hypodynamic cold shock (low cardiac output states). Norepinephrine is the agent of choice for fluid-refractory warm septic shock (hyperdynamic cardiac output, bounding pulses, vasodilation, and wide pulse pressure). Dobutamine improves systolic function and decreases systemic vascular resistance without significantly increasing heart rate, and is effective for patients with cardiomyopathy and congestive heart failure. For patients with adequate blood pressure but with persistent signs of shock, use milrinone or inamrinone to improve cardiac output by reducing afterload due to its vasodilator effects. If the desired effect is not achieved with one agent, combinations of several agents may be necessary.
Epinephrine (0.1–1 mcg/kg/min)
Epinephrine is a potent inotropic agent that effectively increases myocardial perfusion pressure. Low-dose epinephrine (<0.2 mcg/kg/min) stimulates both beta-1 cardiac and beta-2 peripheral vascular receptors, which results in increased heart rate and contractility, decreased systemic vascular resistance (SVR), and decreased diastolic blood pressure. At doses >0.3 mcg/kg/min, alpha-adrenergic vasoconstriction leads to an increase in blood pressure. Epinephrine causes increased myocardial oxygen demand and may lead to myocardial ischemia; however, this is rare in children. An epinephrine infusion is useful for persistent hypotension after cardiopulmonary resuscitation and in low-output septic shock, and its bronchodilator effects are also useful in anaphylactic shock. Since infants are less responsive to dopamine and dobutamine, epinephrine may be superior at maintaining blood pressure and cardiac output. Infuse at an initial rate of 0.1 mcg/kg/min, and titrate to the desired effect.
Norepinephrine (0.1–2 mcg/kg/min)
Norepinephrine acts on both alpha- and beta-adrenergic receptors, producing potent inotropic effects and peripheral vasoconstriction, significantly increasing mean arterial pressure and cardiac contractility, without causing tachycardia. The increased blood pressure also improves renal perfusion in patients with septic shock. Norepinephrine is effective in persistent hypotension after cardiopulmonary resuscitation in patients with low SVR, as in high-output warm shock, anaphylactic shock, and spinal shock. Infuse at an initial rate of 0.1 mcg/kg/min, and titrate to the desired effect.
Dopamine (2 – 20 mcg/kg/min)
Dopamine is an endogenous catecholamine with complex effects on the heart and circulation. At low doses (2 mcg/kg/min) dopamine has relatively little chronotropic effects; the primary result is an increase in renal and splanchnic perfusion. At higher infusion rates, it has positive inotropic and chronotropic effects and tends to increase cardiac output and systemic vascular resistance. Infuse at an initial rate of 5–10 mcg/kg/min and titrate to the desired effect.
Dobutamine (2–20 mcg/kg/min)
Dobutamine has selective action on beta-1 and -2 adrenergic receptors with chronotropic and inotropic actions, along with alpha-adrenergic blocking activity. It is an effective inotrope for the normotensive post-arrest patient with poor perfusion. Dobutamine is particularly useful for patients with congestive heart failure or cardiogenic shock, since it increases cardiac output without significantly increasing heart rate. At a dose >10 mcg/kg/min, dobutamine tends to produce hypotension due to afterload reduction and decreased SVR. The hypotension may then require dopamine or epinephrine to increase the SVR. An alternate approach is to start the patient on norepinephrine or dopamine to stabilize the blood pressure and then switch to dobutamine. Infuse dobutamine at an initial rate of 2–10 mcg/kg/min, and titrate to the desired effect.
Phosphodiesterase inhibitors combine inotropic effects on the myocardium (improved cardiac contractility) with systemic arterial and venous dilation (afterload reduction). They increase cardiac output without causing tachycardia or increasing myocardial oxygen demand. They are beneficial in normotensive fluid-resistant shock in patients with myocardial dysfunction associated with increased systemic and pulmonary vascular resistance. Use either: milrinone 50 mcg/kg loading dose over 10–60 minutes, then infuse at 0.25–0.75 mcg/kg/min; or inamrinone 0.75–1 mg/kg loading dose over 5 minutes, may repeat twice; 3 mg/kg total maximum, then infuse at 5–10 mcg/kg/min.
Medications and Electrical Therapy in Resuscitation
The preferred routes of drug administration are IV or IO. However, if an ETT is placed prior to IV or IO insertion, the following medications can be administered via the ETT: lidocaine, epinephrine, atropine, naloxone (LEAN). Instill the drug directly into the ETT or through a 5 Fr feeding tube that extends beyond the tip of the ETT and follow with a 5 mL normal saline flush.
Provide five manual positive pressure ventilations after drug administration to facilitate drug delivery. Drug absorption via the ETT route is unpredictable, so higher doses are required to achieve appropriate therapeutic levels. For epinephrine, use 0.1 mg/kg (0.1 mL/kg) of the 1:1000 concentration; for other drugs, administer 2–3 times the usual IV dose.
Epinephrine is indicated in cardiac arrest (asystole and pulseless electric activity), and in patients with symptomatic bradycardia who are still hypotensive after volume resuscitation. It increases heart rate, myocardial contractility, systemic vascular resistance, and cardiac automaticity, although it also increases myocardial oxygen demand. The increase in coronary perfusion pressure correlates directly with myocardial blood flow, which is a good predictor of return of spontaneous circulation. With ventricular arrhythmias, epinephrine makes the myocardium more susceptible to successful defibrillation.
The IV/IO dose is 0.01 mg/kg (0.1 mL/kg) of the 1:10,000 concentration every 3–5 minutes as needed (1 mg = 10 mL maximum). The ETT dose is 0.1 mg/kg (0.1 mL/kg) of the 1:1000 concentration every 3–5 minutes. For specific toxins or drug overdoses such as beta-blocker (pp. 462–463) or calcium channel blocker (pp. 464–465), high-dose epinephrine may be used if there is no response after the usual IV/IO dose.
Atropine is a parasympatholytic drug that inhibits vagal activity, accelerates sinoatrial pacemaker, and enhances atrioventricular conduction. Atropine is indicated for symptomatic bradycardia with evidence of poor perfusion or hypotension, secondary to increased vagal tone, cholinergic drug toxicity, or AV heart block. However, since hypoxia is commonly the underlying cause for bradycardia, particularly in infants, efforts to improve oxygenation and perfusion must precede the administration of atropine. If the patient does not respond to atropine despite adequate oxygenation and ventilation, use epinephrine. Give 0.02 mg/kg IV/IO (maximum single dose: 0.5 mg in children, 1 mg in adolescents). Atropine may be repeated once in five minutes. For ETT, use 2–3 times the IV dose.
Check the blood glucose concentration at the bedside with a glucometer, during and after an arrest. Promptly give dextrose if the glucose level is <45 mg/dL in a neonate or <60 mg/dL in an infant or child. Recheck the blood glucose concentration after each administration, and try to avoid excessive hyperglycemia, which is related to increased mortality in critically ill children.
The dose is 0.5–1 g/kg. In neonates, infants, and children under five years of age, use 5 mL/kg of a 10% dextrose solution prepared by diluting D50 W 1:4 with sterile water. For older children, use 2 mL/kg of a 25% dextrose solution or 5 mL/kg of a 10% dextrose solution.
Calcium Chloride 10%, Calcium Gluconate 10%
Routine administration of calcium does not improve outcomes of cardiac arrest, and can antagonize the action of epinephrine and other adrenergic agents. However, calcium is indicated for documented hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdose. Use the measured ionized calcium concentration to determine the need for subsequent doses. Avoid rapid calcium administration, which can cause bradycardia or sinus arrest. In the setting of imminent or ongoing cardiac arrest, calcium chloride is preferred over calcium gluconate because it provides greater bioavailability of calcium. Due to the risk of skin sclerosis, if there is extravasation through a peripheral venous line, administer calcium chloride via a central venous catheter, if possible. Calcium gluconate is otherwise preferred for all non-arrest situations, and it can be administered by peripheral or central venous access.
The dose for calcium chloride is 20 mg/kg (0.2 mL/kg) IV slow; this dose may be repeated once in ten minutes. The dose for calcium gluconate is 60 mg/kg (0.6 mL/kg) IV slow. Flush the line with normal saline before and after calcium administration.
Do not use sodium bicarbonate routinely during cardiopulmonary resuscitation, as it may further depress cardiac contractility and inactivate simultaneously administered catecholamines. Sodium bicarbonate is recommended for symptomatic hyperkalemia, tricyclic antidepressant or sodium channel blocker overdose, or for severe metabolic acidosis or prolonged cardiopulmonary arrest after appropriate ventilation and volume restoration is provided. The dose is 1 mEq/kg (1 mL/kg) slow IV or IO; it cannot be given through ETT. Use a 4.2% solution in infants under six months of age. Sodium bicarbonate causes hypernatremia and hyperosmolarity and, if it extravasates, may cause skin necrosis. IV/IO tubing must be flushed with normal saline before and after giving sodium bicarbonate to prevent precipitation with administered calcium chloride or inactivation of administered epinephrine.
Adenosine is the drug of choice for the treatment of stable supraventricular tachycardia (SVT) (pp. 52–53) if vagal maneuvers are unsuccessful or in unstable SVT while preparations are being made for cardioversion. Administer adenosine rapidly and follow with a rapid push of normal saline using a three-way stopcock through an IV placed as close to the heart as accessible. After a brief period (15–30 seconds) of asystole or heart block, the rhythm either converts to sinus or reverts to SVT. The first dose is 0.1 mg/kg IV/IO (rapid) to a maximum of 6 mg, followed by a 5–10 mL normal saline flush. If needed, the second dose is 0.2 mg/kg IV/IO (12 mg maximum). This dose may be repeated once (total of three doses). If the patient has unstable SVT or deteriorates, immediately attempt synchronized cardioversion. Adenosine is contraindicated in patients with Wolff–Parkinson–White (WPW) syndrome and preexisting second- or third-degree heart block.
Amiodarone (pp. 57–58) is indicated for shock-refractory ventricular tachycardia (VT) or pulseless VT, hemodynamically unstable VT, and stable SVT refractory to adenosine. Avoid administering amiodarone with any other drug that causes QT prolongation (procainamide) or in patients with prolonged QT syndrome, as it may precipitate polymorphic VT.
The loading dose for SVT, VT (with and without pulses), and ventricular fibrillation is 5 mg/kg IV (300 mg maximum) over 20–60 minutes. Repeat this dose every 10 minutes to a maximum total dose of 15 mg/kg/day (2.2 g/day).
Lidocaine (pp. 58–59) is an alternative to amiodarone for VT with pulses and pulseless shock-resistant VF or VT. The initial IV/IO dose is 1 mg/kg (ETT 2–3 mg/kg). This dose may be repeated in 10–15 minutes. If maintenance infusion is required, infuse at 20–50 mcg/kg/min. Lidocaine is contraindicated in WPW syndrome and may cause seizures, myocardial depression, and circulatory shock.
Procainamide (p. 58) is effective in the treatment of atrial fibrillation, atrial flutter, and adenosine-refractory stable SVT (including WPW syndrome) and can be used as an alternative therapy for refractory or recurrent stable VT with pulse. Infuse medication slowly to avoid heart block, myocardial depression, hypotension, or prolongation of the QT interval. Monitor blood pressure and the ECG continuously. If the QRS widens by more than 50% or hypotension develops, stop the infusion. Do not administer concurrently with other medications that prolong the QT interval (amiodarone). The dose is 15 mg/kg IV/IO (1000 mg maximum) over 30–60 minutes followed by a continuous IV infusion at 40–50 mcg/kg/min.
Cardioversion and Defibrillation
Cardioversion is the synchronized electrical conversion of a rhythm disturbance. Synchronized cardioversion is timed with the QRS complex to avoid delivery during the relative refractory period of the cardiac cycle, during which a shock could induce potentially lethal VF. It is indicated for unstable SVT, atrial fibrillation, atrial flutter, monomorphic VT with a pulse, and clinical signs of shock. The first dose is 0.5–1 J/kg (50–100 J maximum). If the initial dose is ineffective, increase subsequent doses to 2 J/kg.
Defibrillation is the delivery of electricity asynchronous to the cardiac cycle, indicated for VF or pulseless VT. Defibrillators are either manual or automated (AED), and deliver monophasic or biphasic waveforms. Place the paddles or self-adhering electrodes on the chest wall, leaving about two fingerbreadths between the paddles. Use infant paddles for children <1 year of age or those weighing <10 kg. Place one paddle over the right side of the upper chest and the other to the left of the nipple on the left lower ribs. Alternatively, apply one electrode on the front of the chest just to the left of the sternum and the other over the upper back below the scapula. Immediately after the shock, resume high-quality CPR for two minutes or five cycles, beginning with chest compressions. Try to limit interruption of CPR for rhythm checks to <10 seconds. If one shock does not convert the rhythm to normal, repeat the process. If VF or VT persists despite delivery of one shock followed by two minutes of CPR, give epinephrine as soon as IV or IO access is available. The first dose for defibrillation is 2 J/kg, then deliver subsequent doses at 4 J/kg.
Shock is defined as a physiologic state characterized by inadequate tissue perfusion to meet metabolic demands and tissue oxygenation. Shock is categorized as hypovolemic, distributive, cardiogenic, and obstructive (Table 1.7). It can be further classified by severity, as compensated or decompensated (hypotensive) shock. In the early phases of shock, multiple compensatory physiologic mechanisms act to maintain blood pressure and perfusion of vital organs (brain, heart, kidneys). If compensatory mechanisms fail and are unable to maintain a systolic blood pressure within a normal range (greater than fifth percentile systolic blood pressure for age), shock is classified as hypotensive. The earlier shock is recognized and treated, the better the patient’s prognosis.
|Type of shock||Etiology|
|Hypovolemic: pump is empty|
|Dehydration (vomiting, diarrhea, poor intake, heat stroke)|
|Hemorrhage (trauma, GI bleed)|
|Metabolic disease (diabetes, adrenal insufficiency)|
|Plasma losses (burns, peritonitis, hypoproteinemia)|
|Cardiogenic: weak/sick pump|
|Congestive heart failure|
|Distributive: fluid distribution problem|
|Neurogenic shock (head trauma, spinal cord injury)|
|Obstructive: obstruction of outflow|
|Ductal-dependent cardiac disease|
The clinical presentation of patients in compensated shock depends on the cardiac output relative to end-organ demand. In infants and children, cardiac output is initially maintained by changes in heart rate, so that the blood pressure may be normal, although there may be tachycardia and irritability. Poor tissue perfusion leads to metabolic acidosis, so that the respiratory rate is increased to promote the excretion of CO2. Therefore, unexplained tachycardia and tachypnea, with a normal blood pressure, and without other signs of shock, may be the earliest signs of cardiorespiratory compromise. Bradycardia and hypotension are ominous, and occur in advanced stages of shock, which can rapidly progress to irreversible multiple organ damage and cardiorespiratory arrest. The signs of shock are summarized in Table 1.8.
|Orthostatic changes||Altered mental status|
|Delayed capillary filling >2 seconds||Markedly delayed capillary filling >4 seconds|
|Adequate central pulse||Weak or absent peripheral pulse|
|Tachypnea||Cold, pale mottled skin|
|Normal blood pressure||Oliguria|
Hypovolemic shock is the most common etiology of shock and refers to a clinical state of reduced intravascular volume. It can be caused by extravascular fluid loss (e.g., diarrhea, dehydration) or intravascular volume loss (e.g., hemorrhage) and results in decreased preload leading to reduced stroke volume and low cardiac output. Tachycardia, increased SVR, and increased cardiac contractility are the primary compensatory mechanisms, resulting in redistribution of intravascular perfusion to the heart, brain, and kidneys. The shunting of blood flow away from the skin causes the changes in skin color, temperature, and moisture seen in compensated shock. Tachypnea is an early finding, as a partial compensation for the metabolic acidosis that accompanies shock. Compensatory mechanisms cannot be maintained indefinitely and bradycardia, myocardial ischemia, hypoxia, and subsequent cardiopulmonary arrest will occur without timely intervention.
Distributive shock refers to a clinical state characterized by reduced SVR leading to maldistribution of blood flow and tissue hypoperfusion. Causes include: septic shock, anaphylactic shock, and neurogenic/spinal shock.
Septic shock is the most common cause of distributive shock. It may evolve over a few hours (particularly in young infants) or days. There is wide variability in clinical presentation and progression, as the cardiac output may be high, normal, or low. Early phases of “warm” septic shock may not be clinically apparent since the skin may be warm and dry without an increase in capillary refill time. This is due to low SVR and cutaneous vasodilation, which result in hyperdynamic cardiac output. Pulses will be rapid, full, and bounding, and the pulse pressure is wide. Normal- or low-output “cold” septic shock is characterized by high SVR and peripheral vasoconstriction, resulting in cold extremities, with weak pulses and delayed capillary refill time.
Anaphylactic shock (pp. 37–41) is an acute multisystem potentially life-threatening response to an allergen involving two or more body systems (cutaneous, respiratory, gastrointestinal, cardiovascular, or neurologic). The reaction is characterized by venodilation, arterial vasodilation, increased capillary permeability, and pulmonary vasoconstriction. The patient presents with some combination of anxiety or agitation, urticaria, nausea and vomiting, wheezing and respiratory distress, angioedema resulting in stridor, and hypotension. Anaphylaxis can progress rapidly (seconds to minutes) to cardiovascular collapse and death.
Neurogenic shock is caused by an acute high spinal cord injury with sudden loss of sympathetic vascular tone, resulting in peripheral vasodilation. Signs of neurogenic shock include: hypotension with a wide pulse pressure, paradoxical bradycardia (absence of compensatory tachycardia), and respiratory distress if the diaphragm is involved. Neurogenic shock may present with flaccid paralysis and loss of bladder and rectal tone. A careful assessment is necessary to differentiate neurogenic shock from other causes of shock. Although patients in neurogenic shock may be warm and well-perfused, they may not respond to either fluid boluses or pressor support.
Cardiogenic shock occurs when cardiac output is compromised secondary to myocardial dysfunction. Common causes include congenital heart disease, arrhythmias, myocarditis, cardiomyopathy, sepsis, toxins, and myocardial injury. Cardiogenic shock is also a terminal complication of virtually all types of shock as a result of high myocardial oxygen requirement and decreased cardiac contractility. Findings consistent with cardiogenic shock are marked tachycardia, normal or low blood pressure with narrow pulse pressure, weak central and peripheral pulses, signs of congestive heart failure (pulmonary edema, hepatomegaly, jugular venous distention), cyanosis, cold, mottled skin, change in level of consciousness, and oliguria. A 12-lead ECG may show low-voltage tachycardia or ST changes, and a chest radiograph reveals cardiomegaly and pulmonary edema. An urgent echocardiogram will determine cardiac function as well as any underlying anatomic defects that may be contributing to the condition.
Obstructive shock refers to conditions that physically impair cardiac output as a result of reduced venous return or limited cardiac contractility. Causes include pericardial tamponade, tension pneumothorax, massive pulmonary embolism, and ductal-dependent congenital heart defects (e.g., coarctation of the aorta, hypoplastic left ventricle). In pericardial tamponade (pp. 758–759), fluid accumulates within the pericardial sac, resulting in increased pericardial pressure and decreased cardiac compliance and cardiac output. Classic signs of cardiac tamponade are tachycardia, poor peripheral perfusion, cool extremities, muffled or diminished heart sounds, narrowed pulse pressure with pulsus paradoxus (decrease in systolic blood pressure by >10 mm Hg during inspiration), and changes in level of consciousness.
In tension pneumothorax (pp. 760–761) free air accumulates within the pleural cavity, causing a mediastinal shift toward the opposite side, collapsing the lung and compromising cardiac output. Patients present with severe respiratory distress, decreased breath sounds on the affected side, tracheal deviation to the contralateral side, shift in the apical cardiac impulse, tachycardia, distended neck veins, pulsus paradoxus, and rapid deterioration in perfusion with cool extremities.
Findings consistent with massive pulmonary embolism are respiratory distress with hypoxia (as a result of ventilation–perfusion mismatch), chest pain, cough with hemoptysis, tachypnea, tachycardia, and hypotension.
Ductal-dependent congenital cardiac anomalies usually present in the first days to weeks of life when the ductus arteriosus closes. Common lesions include coarctation of the aorta, interrupted aortic arch, coarctation, and hypoplastic left heart syndrome. Restoring patency of the ductus arteriosus is critical for survival until surgical intervention is achieved. Neonates present with cyanosis, tachypnea, congestive heart failure, higher preductal versus postductal blood pressure and O2 saturation, absence of femoral pulses (coarctation and interrupted aortic arch), metabolic acidosis, and shock.
Perform an initial assessment of the patient, including the general appearance, mental status and ABCs (see pp. 2–4, Rapid Cardiopulmonary Assessment), a SAMPLE history, and a complete set of vital signs. During the initial assessment, do not delay providing critical interventions, properly position the head, provide supplemental oxygen, and establish IV or IO access.
Since the signs of early shock are subtle, maintain a high index of suspicion. Be alert to tachycardia, tachypnea, delayed capillary refill (>2 seconds), orthostatic changes in blood pressure or pulse, and irritability. Patients with septic shock may have hypothermia or hyperthermia, altered mental status, irritability or lethargy, and peripheral vasodilation with bounding pulses (warm shock) or mottled cool extremities with thready pulses (cold shock).
If cardiogenic shock is suspected, obtain a 12-lead ECG, which may show low-voltage tachycardia or ST changes; a chest radiograph reveals cardiomegaly and pulmonary edema. An urgent echocardiogram will determine cardiac function as well as any underlying anatomic defects that may be contributing to the condition.
Warning signs that indicate progression from compensated to decompensated (hypotensive) shock include increasing tachycardia, diminishing or absent peripheral pulses, weakening central pulses, narrowing pulse pressure, cold distal extremities with prolonged capillary refill, and decreasing level of consciousness.
ED Management (Figure 1.4)
The most common error in treating shock is underestimating the severity of the condition. Tachycardia that is unexplained by pain or fever is always concerning. If compensated shock is suspected, treat promptly and aggressively to prevent progression to hypovolemic shock. All patients require secure vascular access, oxygen therapy, and cardiopulmonary monitoring. The goals of initial management are to restore normal mental status, heart rate and blood pressure, good peripheral perfusion, and adequate urine output. Early identification of the etiology will help to treat reversible causes.
Position. Allow a conscious patient to assume a position of comfort. If hypotensive, place the child in the Trendelenburg position, unless breathing is compromised.
Oxygenation and Ventilation. For spontaneously breathing patients, administer high-concentration oxygen via nonrebreather mask. Other interventions may include noninvasive positive airway pressure (BiPAP, CPAP) in awake and cooperative patients, or assisted ventilation with a bag-mask device or mechanical ventilation with PEEP if there is evidence of airway compromise.
Establish Vascular Access. Establish two large-bore peripheral IV lines or place a central catheter. If venous access is not possible or delayed, use an IO needle. In critically ill or injured patients, do not spend more than 1–2 minutes attempting to establish peripheral vascular access. The effort may be resumed after the IO line is secured.
Fluid Resuscitation. Give isotonic crystalloid (NS or LR) 20 mL/kg IV bolus over 5–20 minutes, and repeat as needed to restore blood pressure and tissue perfusion. If there is a concern for cardiogenic shock, use smaller fluid boluses of 5–10 mL/kg given over 10–20 minutes. Carefully monitor for signs of pulmonary edema or worsening tissue perfusion, and stop the infusion if any of these occur.
Consider blood transfusion in cases of blood loss or other causes of severe anemia. Trauma victims may require blood transfusion of packed RBCs (10 mL/kg) to replace ongoing losses; use cross-matched, type-specific or O-negative blood. Trauma patients who remain hypotensive despite fluid resuscitation require immediate operative intervention.
Medication and Pressor Infusion. The patient might need pharmacologic support to improve cardiac output, correct metabolic derangements, and/or manage pain and anxiety. If the patient remains hypotensive after initial fluid resuscitation of 40–60 mL/kg, an inotropic agent or a combination of several agents may be necessary to stabilize blood pressure (pp. 23–25). Titrate the dose to the desired effect. Monitor the patient carefully and wean off pressors once blood pressure has improved.
Laboratory Studies. Laboratory studies (i.e., CBC, glucose, potassium, calcium, lactate, blood gas analysis) provide important information to help identify the etiology and severity of shock, evaluate organ dysfunction and metabolic derangements, and assess the response to therapy. Check bedside glucose and treat hypoglycemia (neonate <45 mg/dL; infant, child, and adolescent <60 mg/dL) with an IV glucose bolus.
Monitoring and Reassessment. Assess and continuously reassess the effectiveness of fluid resuscitation and medication therapy. Initiate noninvasive monitoring, including the level of consciousness, heart rate, blood pressure, SpO2, and temperature. Insert a Foley catheter and monitor urine output; the goal is 0.5–1 mL/kg/h, or about 30 mL/h in adolescents. Recognize any limitations in the care and call for help when needed. Early subspecialty consultation (e.g., pediatric critical care, pediatric cardiology, pediatric surgery) is an essential component of shock management and may influence outcome.
Management of Shock According to Cause (Figure 1.5)
Non-hemorrhagic. Give an isotonic crystalloid 20 mL/kg bolus, and repeat as needed. Colloid may be necessary
Hemorrhagic. Control the external bleeding and initially give 3 mL of isotonic crystalloid for every 1 mL of estimated blood lost. Once blood is available, transfuse packed RBCs (10 mL/kg) to replace ongoing losses; use cross-matched, type-specific, or O-negative blood.
Septic Shock. Administer isotonic crystalloid, 20 mL/kg bolus rapidly, up to 60mL/kg in the first hour. Administer antibiotic therapy as soon as possible, preferably within the first 60 minutes. Send the appropriate cultures, but do not delay antibiotic therapy if cultures are not readily obtained. See pp. 391–393 for empiric antibiotic choices and doses.
Anaphylactic Shock. The management is summarized on pp. 38–40. Effective treatment involves early recognition of symptoms of anaphylaxis and anticipating the need for advanced airway techniques.
Neurogenic Shock. Position the patient child flat or head-down. Administer a trial of bolus of isotonic crystalloid (20 mL/kg) and repeat as necessary. For fluid-refractory hypotension, use vasopressors. Provide supplementary warming or cooling as needed.
Rapid volume resuscitation of cardiogenic shock in the setting of poor myocardial function can aggravate pulmonary edema and further impair myocardial function, compromising oxygenation, ventilation, and cardiac output. Administer gradual volume resuscitation with 5–10 mL/kg boluses of isotonic crystalloid delivered over a longer period of time. Carefully monitor hemodynamic parameters during fluid infusion, and repeat the infusion as needed to maintain tissue perfusion. Children with cardiogenic shock often require vasopressor medications to increase and redistribute cardiac output, improve myocardial function, and reduce SVR. The treatment of congestive heart failure (pp. 68–69) and dysrhythmias (pp. 47–62) is detailed elsewhere.
The goals of post-resuscitation care (Figure 1.4) are to preserve brain function, avoid secondary organ injury, and to diagnose and treat the cause of illness. Ultimate outcome after resuscitation is often determined by the subsequent care the child receives. The first phase in post-resuscitative management is to continue to provide advanced life support for immediate life-threatening conditions and focus on the ABCs. The second phase provides broader multiorgan supportive care. When the patient is stable, transfer to a pediatric center if locally there is inadequate pediatric emergency and critical care expertise.
Providing Adequate Oxygenation and Ventilation. Titrate the inspired oxygen to maintain an O2 saturation ≥94–99%) and maintain acceptable PaCO2 levels (<45 mm Hg). For an intubated patient, verify tube position, obtain ABGs, and adjust ventilatory settings as necessary. Use the DOPE mnemonic (Displaced, Obstructed, Pneumothorax, Equipment failure) to assess clinical deterioration in an intubated patient.
Supporting Tissue Perfusion and Cardiovascular Function. Post-resuscitation patients are often poorly perfused as a result of ongoing fluid loss, decreased cardiac function, and alterations in SVR. Give parental fluids and vasoactive agents to maintain the systolic blood pressure above the fifth percentile for age. Monitor mental status, skin perfusion, pulse quality, and blood pressure. Place a urinary catheter to monitor urine output (>0.5–1 mL/kg/h in infants and children; >30 mL/h in adolescents).
Maintaining Adequate Glucose Concentration. Check glucose early and treat as needed. Avoid hyperglycemia and use a target glucose level of <150 mg/dL.
Correcting Acid–Base and Electrolyte Imbalances. Patients usually have metabolic acidosis, which responds to adequate fluid therapy. The routine use of sodium bicarbonate is not indicated.
Temperature Regulation. Maintain a normal temperature and avoid hyperthermia by treating fever (>38 °C). Provide warming devices for hypothermic infants. For a comatose patient resuscitated from an out-of-hospital cardiac arrest, maintain either five days of normothermia (36–37.5 °C) or two days of initial continuous hypothermia (32–34 °C) followed by three days of normothermia. For a patient who remains comatose after in-hospital cardiac arrest, there is insufficient data to recommend hypothermia over normothermia.
Ensure Adequate Analgesia and Sedation (pp. 715–722). Control pain and discomfort with analgesics (fentanyl or morphine) and sedatives (lorazepam or midazolam).
Family Presence During Resuscitation
Presence of family members during in-hospital resuscitation appears to be beneficial and helps in their own adjustment and grieving process, and does not negatively impact staff performance. Healthcare providers should offer the opportunity to be present, whenever possible. However, gently ask family members to leave if they become disruptive to the resuscitation team. Have a member of the resuscitation team stay with the family to inform them of the progress of resuscitation efforts, offer an explanation of events, answer questions, and offer comfort.
Termination of Resuscitation
There are no reliable predictors of when to stop resuscitative efforts after in-hospital pediatric cardiac arrest. In the past, children who underwent prolonged resuscitation without return of spontaneous circulation after two doses of epinephrine were considered unlikely to survive, although neurologically intact survival has been documented. Offer prolonged resuscitative efforts for patients with recurring or refractory VF/VT, drug toxicity, or a primary hypothermic insult. Witnessed collapse, bystander CPR, and a short interval from collapse to arrival of EMS improve the chance of survival. Some predictors of poor outcome in infants and children with out-of-hospital cardiac arrest are: age <1 year, longer duration of cardiac arrest, and presentation with a nonshockable rhythm.
When resuscitation efforts are terminated, arrange for the team leader to meet with family members in order to comfort and apprise them of the resuscitation efforts. Soon afterwards, have the senior members organize a debriefing of the resuscitation team in order to acknowledge the contributions of the team and review the resuscitation efforts.