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					27/04/2011                              Guidelines for pediatric advanced life s…

                               Official reprint from UpToDate® www.uptodate.com
                                                  ©2011 UpToDate®



  Guidelines for pediatric advanced life support
  Authors                               Section Editor                          Deputy Editor
  Eric Fleegler, MD, MPH                Susan B Torrey, MD                      James F Wiley, II, MD, MPH
  Monica Kleinman, MD


  Last literature review version 19.1: enero 2011 |                This topic last updated: febrero 17, 2011
  INTRODUCTION — The American Heart Association (AHA) Pediatric Advanced Life Support (PALS)
  program provides a structured approach to the assessment and treatment of the critically ill
  pediatric patient [1]. The AHA guidelines for pediatric resuscitation were updated in 2010 to reflect
  advances and research in clinical care using new evidence from a variety of sources ranging from
  large clinical trials to animal models [2]. The PALS content includes:

         Overview of assessment
         Recognition and management of respiratory distress and failure
         Recognition and management of shock
         Recognition and management of cardiac arrhythmias
         Recognition and management of cardiac arrest
         Post resuscitation management of patients with pulmonary and cardiac arrest
         Review of pharmacology

  The clinician should primarily focus on prevention of cardiopulmonary failure through early
  recognition and management of respiratory distress, respiratory failure, and shock that can lead to
  cardiac arrest from hypoxia, acidosis, and ischemia.

  This topic will discuss the advanced components of recognition and treatment of respiratory failure,
  shock, cardiopulmonary failure, and cardiac arrhythmias in children. Basic life support in children and
  guidelines for cardiac resuscitation in adults are discussed separately. (See "Basic life support in
  infants and children" and "Advanced cardiac life support (ACLS) in adults".)

  OVERVIEW OF ASSESSMENT — The assessment of respiratory distress and circulatory compromise
  in children, including the common findings, is covered in greater detail separately. (See "Initial
  assessment and stabilization of children with respiratory or circulatory compromise".)

  PALS uses an assessment model that facilitates rapid evaluation and intervention for life-
  threatening conditions. In infants and children, most cardiac arrests result from progressive
  respiratory failure and/or shock, and one of the aims of this rapid assessment model is to prevent
  progression to cardiac arrest. The evaluation includes:

         General assessment via the pediatric assessment triangle (brief visual and auditory
         observation of child's overall appearance, work of breathing, circulation) (see "Initial
         assessment and stabilization of children with respiratory or circulatory compromise")

         Primary assessment (rapid evaluation of cardiopulmonary and neurologic function)

         Secondary assessment (focused medical history using SAMPLE mnemonic and thorough head
         to toe physical exam)

         Tertiary assessment (laboratory, radiographic, and other ancillary studies)
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  Primary assessment — The clinician should in rapid sequence assess:

         Airway (patent, patent with maneuvers/adjuncts, partially or completely obstructed)

         Breathing (respiratory rate, effort, tidal volume, lung sounds, pulse oximetry)

         Circulation (skin color and temperature, heart rate and rhythm, blood pressure, peripheral and
         central pulses, capillary refill time)

         Disability

             AVPU pediatric response scale: Alert, Voice, Pain, Unresponsive

         Glasgow Coma Scale: Eye Opening, Verbal Response, Motor Response (table 1)

             Pupillary response to light
             Presence of hypoglycemia (rapid bedside glucose or response to empiric administration of
             dextrose)

         Exposure (fever or hypothermia, skin findings, evidence of trauma)

  Secondary assessment — This portion of the evaluation includes a thorough head to toe physical
  examination, as well as a focused medical history that consists of the "SAMPLE" history:

         S: Signs and symptoms
         A: Allergies
         M: Medications
         P: Past medical history
         L: Last meal
         E: Events leading to current illness

  Tertiary assessment — Injury and infection are common causes of life-threatening illness in
  children. Thus, ancillary studies are frequently directed towards identifying the extent of trauma or
  an infectious focus. (See "Trauma management: Approach to the unstable child", section on
  'Adjuncts to the primary survey' and "Trauma management: Approach to the unstable child", section
  on 'Adjuncts to the secondary survey' and "Approach to the septic-appearing infant", section on
  'Ancillary studies' and "Initial evaluation of shock in children", section on 'Evaluation'.)

  RESPIRATORY DISTRESS AND FAILURE — A major goal of PALS is to recognize and treat
  respiratory conditions amenable to simple measures (eg, supplemental oxygen, inhaled albuterol).
  The clinician may also have to treat rapidly progressive conditions and intervene with advanced
  therapies to avoid cardiopulmonary arrest in patients with respiratory failure. Early detection and
  treatment improve overall outcome.

  There are many causes of acute respiratory compromise in children (table 2). The clinician should
  strive to categorize respiratory distress or failure into one or more of the following (see "Emergent
  evaluation of acute respiratory distress in children"):

         Upper airway obstruction (eg, croup, epiglottitis)
         Lower airway obstruction (eg, bronchiolitis, status asthmaticus)
         Lung tissue (parenchymal) disease (eg, bronchopneumonia)
         Disordered control of breathing (eg, seizure, coma, muscle weakness)


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  Initial management supports airway, breathing, and circulation:

         Airway - Key steps in basic airway management include (see "Basic airway management in
         children"):

             Provide 100 percent inspired oxygen
             Allow child to assume position of comfort or manually open airway
             Clear airway (suction)
             Insert oropharyngeal airway or nasopharyngeal airway if consciousness impaired

         Breathing - The clinician should assist ventilation manually in patients not responding to basic
         airway maneuvers, monitor oxygenation by pulse oximetry, monitor ventilation by end-tidal
         CO2 if available, and administer medications as needed (albuterol, epinephrine). In preparation
         for intubation, positive pressure ventilation should be initiated with a bag-valve-mask to
         preoxygenate and improve ventilation. (See "Basic airway management in children".)

         Children who cannot maintain their airway, oxygenation, or ventilatory requirements should
         undergo placement of an artificial airway, usually via endotracheal intubation and less
         commonly with a laryngeal mask airway or alternative device. A rapid overview describes the
         steps in performing rapid sequence intubation (table 3). (See "Emergent endotracheal
         intubation in children" and "Rapid sequence intubation in children".)

         Circulation - Key interventions consist of monitoring heart rate and rhythm and establishing
         vascular access (see "Vascular (venous) access for pediatric resuscitation and other pediatric
         emergencies").

  SHOCK — The goal is to recognize and categorize the type of shock in order to prioritize treatment
  options (algorithm 1). Early treatment of shock may prevent the progression to cardiopulmonary
  failure (algorithm 2).

  Shock results from the inadequate delivery of oxygen to the tissues relative to tissue metabolic
  demand, usually characterized by inadequate perfusion. Shock may occur with normal, increased, or
  decreased systolic blood pressure. Shock in children is usually related to low cardiac output, but
  some patients may have high cardiac output, such as with sepsis or severe anemia. (See "Initial
  evaluation of shock in children".)

  Shock severity is usually categorized by its effect on systolic blood pressure:

         Compensated shock occurs when compensatory mechanisms (including tachycardia, increased
         systemic vascular resistance, increased inotropy, and increased venous tone) maintain a
         systolic blood pressure within a normal range (table 4).

         Hypotensive shock (or decompensated shock) occurs when compensatory mechanisms fail to
         maintain systolic blood pressure. In children 1 to 10 years of age, hypotension is defined as a
         systolic pressure of <70 mmHg + (child's age in years x2) mmHg. Compensated shock may
         take hours to progress to hypotensive shock. Hypotensive shock may progress to
         cardiopulmonary failure in minutes.


         Shock categorization – There are four major categories of shock (see "Initial evaluation of
         shock in children"):

             Hypovolemic shock - Hypovolemic shock is characterized by inadequate circulating blood
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             volume. Common causes of fluid loss include diarrhea, hemorrhage (internal and external),
             vomiting, inadequate fluid intake, osmotic diuresis (eg, diabetic ketoacidosis), third-space
             losses, and burns.
             Distributive shock - Distributive shock describes inappropriately distributed blood volume
             typically associated with decreased systemic vascular resistance. Common causes include
             septic shock, anaphylactic shock, and neurogenic shock (eg, head injury, spinal injury).
             Cardiogenic shock - Cardiogenic shock refers to impairment of heart contractility. Common
             causes include congenital heart disease, myocarditis, cardiomyopathy, arrhythmias,
             sepsis, poisoning or drug toxicity, and myocardial injury (trauma).
             Obstructive shock - In this form of shock, hypotension arises from obstructed blood flow
             to the heart. Common causes include cardiac tamponade, tension pneumothorax, ductal
             dependent congenital heart lesions, and massive pulmonary embolism.

             Any given patient may suffer from more than one type of shock. For example, a child in
             septic shock may develop hypovolemia during the prodrome phase, distributive shock
             during the early phase of sepsis, and cardiogenic shock later in the course.

         Shock management – The approach to undifferentiated shock in children requires careful
         attention to history and physical examination in order to arrive at the type of shock present
         (algorithm 2). Goal-directed therapy for shock is discussed separately. (See "Initial
         management of shock in children", section on 'Early goal-directed therapy'.)

         Early treatment can greatly improve outcome. Goals are to improve oxygen delivery and to
         reduce oxygen consumption. Specific measures include increasing circulating volume,
         increasing cardiac contractility, improving distribution of cardiac output, and reducing oxygen
         demand. Methods include:

             Administration of high concentration of oxygen
             Support of respirations to decrease the work of breathing
             If rapid sequence intubation is necessary, an sedating agent should be chosen so that
             hemodynamic stability is not worsened (see "Initial management of shock in children",
             section on 'Airway management')
             Rapid intravenous administration of fluids (eg, boluses of normal saline 20 mL/kg up to
             three times or more as needed for persistent hypotension)
             Administration of vasoconstrictors in selected patients
             Use of inotropic medications in selected patients
             Transfusion
             Reversal of identified obstructions
             Other adjunct methods include treatment of underlying infection, fever, pain and anxiety,
             and treatment of metabolic derangements (hypoglycemia, hypocalcemia, hyperkalemia,
             metabolic acidosis)

  CARDIOPULMONARY FAILURE — Respiratory failure and hypotensive shock are the most common
  conditions preceding cardiac arrest.

         Causes of respiratory failure include:

             Upper airway obstruction (choking, infection)

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             Lower airway obstruction (asthma, foreign body aspiration)
             Parenchymal disease (pneumonia, acute pulmonary edema)

         Causes of hypotensive shock include:

             Hypovolemia (dehydration, hemorrhage)
             Cardiac disease
             Distributive shock (septic, neurogenic)
             Metabolic/electrolyte disturbances
             Acute myocardial infarction/ischemia
             Toxicologic ingestions
             Pulmonary embolism

         The following physical findings often precede cardiopulmonary failure:

             Airway - Possible upper airway obstruction secondary to decreased level of
             consciousness or anatomic obstruction from foreign body or infection
             Breathing - Bradypnea, irregular, ineffective respiration, gasping
             Circulation - Bradycardia, capillary refill >5 seconds, weak central pulses, no peripheral
             pulses, hypotension, cool extremities, mottled/cyanotic skin
             Disability - Diminished level of consciousness

  The patient in cardiopulmonary failure will progress rapidly to cardiac arrest without aggressive
  intervention. Positive pressure ventilations with 100 percent inspired oxygen, chest compressions
  for heart rate <60 beats per minute in patients with poor perfusion, and administration of
  intravenous fluids and medications tailored to treat the underlying cause are indicated. (See "Basic
  airway management in children" and "Basic life support in infants and children".)

  APPROACH TO CARDIAC ARRHYTHMIAS — Arrhythmias are classified as bradyarrhythmias,
  tachyarrhythmias, and pulseless arrest. Evaluation requires knowledge of the child's typical heart
  rate (table 4) and baseline rhythm as well as level of activity and clinical condition. The approach
  presented here is based on the consensus 2010 international resuscitation guidelines developed by
  the American Heart Association (AHA) and the International Liaison Committee on Resuscitation
  (ILCOR) [3-5].

  BRADYARRHYTHMIAS

         Definition — Bradycardia is defined as a heart rate that is slow compared with normal heart
         rates for the patient's age (table 4). Primary bradycardia is the result of congenital and
         acquired heart conditions that directly slow the spontaneous depolarization rate of the heart's
         pacemaker or slow conduction through the heart's conduction system. Secondary bradycardia
         is the result of conditions that alter the normal function of the heart, including hypoxia,
         acidosis, hypotension, hypothermia, and drug effects. Bradyarrhythmias are common prearrest
         rhythms in children and are often due to hypoxia.

         Signs and symptoms — Pathologic bradycardia frequently causes a change in the level of
         consciousness, lightheadedness, dizziness, syncope, or fatigue. Shock associated with
         bradycardia can manifest with hypotension, poor end-organ perfusion, altered consciousness,
         and/or sudden collapse. Bradycardia with symptoms of shock (eg, poor systemic perfusion,
         hypotension, altered consciousness) requires urgent treatment to prevent cardiac arrest. ECG
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         findings associated with bradycardia include (see "Bradycardia in children"):

             Slow heart rate relative to normal rates (table 4)
             P waves that may or may not be visible
             QRS complex that is narrow (electrical conduction arising from the atrium or high nodal
             area) or wide (electrical conduction from low nodal or ventricular region)
             P wave and QRS complex may be unrelated (ie, atrioventricular dissociation) or have an
             abnormally long period between them (atrioventricular block)

  Sinus bradycardia — Sinus bradycardia is commonly an incidental finding in healthy children as a
  normal consequence of reduced metabolic demand (sleep, rest) or increased stroke volume (well-
  conditioned athlete). Pathologic causes include hypoxia, hypothermia, poisoning, electrolyte
  disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased
  intracranial pressure. (See "Bradycardia in children", section on 'Sinus bradycardia'.)

  Atrioventricular block — Atrioventricular (AV) block is defined as a delay or interruption in the
  transmission of an atrial impulse to the ventricles due to an anatomical or functional impairment in
  the conduction system. Heart block is categorized into three types:

         First degree — First degree AV block is characterized by a prolonged PR interval for age
         caused by slow conduction through the AV node without missed ventricular beats (figure 1).
         Of note, first degree AV block does not cause bradycardia. In general, the normal PR-intervals
         are: 70 to 170 msec in newborns, and 80 to 220 msec in young children and adults. (See
         "Bradycardia in children", section on 'First-degree AV block'.)

         Second degree — In second-degree AV block, the organized atrial impulse fails to be
         conducted to the ventricle in a 1:1 ratio. There are two types of second degree AV block
         (see "Bradycardia in children", section on 'Second-degree AV block'):

         Mobitz type I (Wenckebach phenomenon) — On ECG, there is progressive prolongation of the
         PR-interval until a P wave fails to be conducted (figure 2). The block is located at the level of
         the AV node and is usually not associated with other significant conduction system disease or
         symptoms.

         Mobitz type II — This block occurs below the AV node and has consistent inhibition of a
         specific proportion of atrial impulses, usually with a 2:1 atrial to ventricular rate (figure 3). It
         has a less predictable course and frequently progresses to complete heart block.

         Third degree — In third-degree AV block, also referred to as complete heart block, there is
         complete failure of the atrial impulse to be conducted to the ventricles (figure 4). The atrial
         and ventricular activity are independent of one another. The ventricular escape rhythm that
         is generated is dictated by the location of the block. It is usually slower than the lower limits
         of normal for age, resulting in clinically significant bradycardia. (See "Bradycardia in children",
         section on 'Third-degree AV block'.)

  Bradyarrhythmia management — The management of bradycardia focuses on reestablishing or
  optimizing oxygenation and ventilation, supporting circulation with chest compressions if needed,
  and using medications to increase heart rate and cardiac output (algorithm 3). If these measures
  fail, transcutaneous pacing can be attempted; however, the same factors that are producing
  refractory bradycardia (eg, hypoxia, hypothermia, electrolyte disturbance, drug overdose) may
  prevent effective electrical capture. (See "Bradycardia in children", section on 'Acute
  management'.)

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  TACHYARRHYTHMIAS

         Definition — Tachyarrhythmias are fast abnormal rhythms originating in the atria or the
         ventricles. Relative tachycardia is a heart rate that is too fast for the child's age, level of
         activity, and clinical condition (table 4). In children, sinus tachycardia usually represents
         hypovolemia, fever, physiologic response to stress or fear, or drug effect (such as with beta
         agonists). (See "Approach to the child with tachycardia".)

         Certain arrhythmias, such as supraventricular tachycardia and ventricular tachycardia, can
         lead to shock and cardiac arrest. Unstable rhythms lead to poor tissue perfusion with a fall in
         cardiac output, poor coronary artery perfusion, and increased myocardial oxygen demand,
         which can all lead to cardiogenic shock.


         Signs and symptoms — Clinical findings in children with tachycardia are often nonspecific and
         vary by age. They may include palpitations, lightheadedness, dizziness, fatigue and syncope.
         In infants, prolonged tachycardia may cause poor feeding, tachypnea, and irritability with
         signs of heart failure. (See "Approach to the child with palpitations" and "Emergent evaluation
         of syncope in children and adolescents".)

         Important ECG findings include:

             Heart rate that is fast compared with normal rates (table 4)
             P waves that may or may not be visible
             QRS interval that is narrow or wide

         Classification — Treatment priorities in managing tachycardias rely on differentiating between
         tachycardia with narrow QRS complex (sinus tachycardia, supraventricular tachycardia, atrial
         flutter) and wide QRS complex tachycardias (ventricular tachycardia, supraventricular
         tachycardia with aberrant intraventricular conduction).

  Sinus tachycardia — Sinus tachycardia is characterized by a rate of sinus node discharge that is
  faster than normal for the patient's age (table 4). This rhythm usually represents the body's
  increased need for cardiac output or oxygen delivery. The heart rate is not fixed and varies with
  other factors, including fever, stress, and level of activity. Causes include tissue hypoxia,
  hypovolemia, fever, metabolic stress, injury, pain, anxiety, toxins/poisons/drugs, and anemia. Less
  common causes include cardiac tamponade, tension pneumothorax, and thromboembolism. (See
  "Approach to the child with tachycardia".)

  Typical ECG findings in patients with sinus tachycardia include:

         Heart rate is usually <220/min in infants, <180/min in children, and exhibits beat to beat
         variability in rate
         P waves are present with normal appearance
         PR interval is constant and exhibits a normal duration for age
         R-R interval is variable
         QRS complex is narrow

  Supraventricular tachycardia — Supraventricular tachycardia (SVT) can be defined as an
  abnormally rapid heart rhythm originating above the ventricles, often (but not always) with a
  narrow QRS complex; it conventionally excludes atrial flutter and atrial fibrillation. The two most
  common forms of SVT in children are atrioventricular reentrant tachycardia (AVRT), including the
  Wolff-Parkinson-White (WPW) syndrome (figure 5), and atrioventricular nodal reentrant tachycardia
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  (AVNRT).

         Signs and symptoms — SVT typically has an abrupt and intermittent presentation. Signs and
         symptoms in infants include poor feeding, tachypnea, irritability, increased sleepiness,
         diaphoresis, pallor, and/or vomiting. Older children may have palpitations, shortness of breath,
         chest pain/discomfort, dizziness, lightheadedness, and/or fainting. Infants and children with
         prolonged SVT may display clinical findings of heart failure. (See "Supraventricular tachycardia
         in children: AV reentrant tachycardia (including WPW) and AV nodal reentrant tachycardia",
         section on 'Clinical features'.)

         Typical ECG findings in patients with SVT include (figure 5) (see "Causes of wide QRS complex
         tachycardia in children", section on 'Supraventricular tachycardia'):

             Heart rate that is usually >220/min in infants, >180/min in children, and has NO beat to
             beat variability
             P waves are absent or abnormal
             PR interval may not be present or short PR interval with ectopic atrial tachycardia
             R-R interval is usually constant
             QRS is usually narrow. Conduction delay along the ventricular system may lead to an
             appearance of wide complex tachycardia, known as SVT with aberrant conduction.

  Ventricular tachycardia — Ventricular tachycardia (VT) originates from the ventricular
  myocardium or Purkinje cells below the bifurcation of the bundle of His (figure 6). VT is associated
  with sudden cardiac death. As a result, patients who develop VT or at risk for developing VT must
  be identified, evaluated, and treated if necessary. Some forms of VT found primarily in infants and
  young children may be benign, but this conclusion is reached only after other more serious causes
  of VT are excluded. VT may present with or without pulses. (See "Causes of wide QRS complex
  tachycardia in children", section on 'Ventricular tachycardia' and 'Pulseless arrest' below.)

  VT with pulses can vary in rate from near normal to >200 beat per minute. Faster rates can
  compromise stroke volume and cardiac output leading to pulseless VT or ventricular fibrillation (VF).
  Causes of VT include underlying heart disease or cardiac surgery, prolonged QT syndrome, or
  myocarditis/cardiomyopathy. Other causes include hyperkalemia and toxic ingestions (eg, tricyclic
  antidepressants, cocaine) (table 5).

  Findings of ventricular tachycardia on ECG include (figure 6):

         Ventricular rate is >120 beats per minute and regular
         P waves are often not identifiable, may have AV dissociation, or may have retrograde
         depolarization
         QRS is typically wide (>0.09 sec)
         T waves are often opposite in polarity from the QRS complex

  Tachyarrhythmia management — The management of sinus tachycardia focuses on treatment of
  the underlying physiologic derangement and is largely supportive. The management of
  tachyarrhythmias that are not sinus in origin is guided by the appearance of the QRS complex, and
  by the patient's status, whether compensated or uncompensated (algorithm 4):

         Patients with either narrow or wide complex tachycardia who have significantly impaired
         consciousness and hypotensive shock should be treated with synchronized cardioversion
         (Initial dose: 0.5 to 1 J/kg). (See "Defibrillation and cardioversion in children (including
         automated external defibrillation)", section on 'Methods: Manual defibrillator use'.)

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         Patients who are mentating and not hypotensive may receive a trial of anti-arrhythmic
         therapy, based on whether the arrhythmia is believed to originate from above the AV node
         (narrow complex, eg, adenosine; initial dose: 0.1 mg/kg) or below the AV node (wide complex,
         eg, amiodarone 5 mg/kg). (See "Management of supraventricular tachycardia in children",
         section on 'Antiarrhythmic drugs' and "Management and evaluation of wide QRS complex
         tachycardia in children", section on 'Initial management'.)

  PULSELESS ARREST — Pulseless arrest refers to cessation of blood circulation caused by absent or
  ineffective cardiac mechanical activity.

  Most pediatric cardiac arrests are hypoxic/asphyxial arrests that result from a progression of
  respiratory distress, respiratory failure, or shock rather than from primary cardiac arrhythmias
  ("sudden cardiac arrest"). Thus, the presenting rhythm is typically asystole.

  Children with pulseless arrest appear apneic or display a few agonal gasps. They have no palpable
  pulses, and are unresponsive. Overall survival from pediatric cardiac arrest is poor, and the
  incidence of neurologic deficits in survivors is high.

  Epidemiology and presenting rhythm — Out-of-hospital arrests in children six months to young
  adulthood often occur at or near home. The most common cause of death is from trauma, leading
  to respiratory compromise and/or shock. Massive head injury and severe multiple systems trauma
  are common in nonsurvivors. Sudden infant death syndrome (SIDS) is a leading cause of death in
  infants <6 months.

  Sudden collapse due to VF/pulseless VT occurs in up to 18 percent of all pediatric prehospital
  cardiac arrests but is less commonly the presenting rhythm in younger children between the ages of
  one and eight years (7.6 percent) [6]. Predisposing conditions or causes of ventricular rhythms in
  pediatric patients with pulseless arrest include hypertrophic cardiomyopathy, anomalous coronary
  artery (from the pulmonary artery), long QT syndrome, myocarditis, drug intoxication (eg, digoxin,
  ephedra, cocaine), and commotio cordis (ie, sharp blow to chest). These patients may have intact
  survival if defibrillation is performed within minutes of arrest.

  For in-hospital cardiac arrest, shockable rhythms are present at some point during the resuscitation
  in 27 percent of children, with 10 percent having VF/VT as the initial arrest rhythm. Survival is
  higher if VF or VT is the presenting arrhythmia (35 percent survival) versus "non-shockable"
  rhythms, such as asystole (11 percent) (algorithm 5) [7].

  Arrest rhythms — Asystole, pulseless electrical activity (PEA), ventricular fibrillation (VF), and
  pulseless ventricular tachycardia (VT) comprise the potential arrest rhythms.

      Asystole — Children with asystole have cardiac standstill with no discernible electrical activity
  (figure 7). The most common cause is respiratory failure progressing to critical hypoxemia,
  bradycardia, and then cardiac standstill. Underlying conditions include pneumonia, submersion,
  hypothermia, sepsis, and poisoning (eg, carbon monoxide poisoning, sedative-hypnotics) leading to
  hypoxia and acidosis.

     Pulseless electrical activity — Pulseless electrical activity (PEA) consists of any organized
  electrical activity observed on ECG in a patient with no central palpable pulse. Reversible conditions
  may underlie PEA, including:

         Hypovolemia
         Hypoxia
         Hydrogen ion (acidosis)
         Hypo-/hyperkalemia
         Hypoglycemia
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         Hypothermia
         Toxins
         Tamponade, cardiac
         Tension pneumothorax
         Thrombosis (coronary or pulmonary)
         Trauma

  These can be remembered as the H's and T's of PEA [2].

     Ventricular fibrillation — Ventricular fibrillation is characterized by no organized rhythm and no
  coordinated contractions (figure 7). Electrical activity is chaotic. Causes overlap with etiologies of
  ventricular tachycardia, including hyperkalemia, congenital or acquired heart disease, toxic
  exposures, electrical or lightning shocks, and submersion.

     Pulseless ventricular tachycardia — Pulseless VT is a cardiac arrest of ventricular origin
  characterized by organized, wide QRS complexes (figure 6). Any cause of VT with pulses can lead
  to pulseless VT. (See 'Ventricular tachycardia' above.)

     Torsades de pointes — Torsades de pointes or polymorphic VT displays a QRS complex that
  changes in polarity and amplitude, appearing to rotate around the ECG isoelectric line (translation:
  "twisting of the points") (figure 8). This arrhythmia is associated with markedly prolonged QTc
  interval from congenital conditions (long QT syndrome), drug toxicity (antiarrhythmic drugs, tricyclic
  antidepressants, calcium channel blockers, phenothiazine), and electrolyte disturbances (eg,
  hypomagnesemia arising from anorexia nervosa). Ventricular tachycardia, including torsades de
  pointes, can deteriorate into ventricular fibrillation.

  Management — For highly effective chest compressions, the individual performing the
  compressions needs to push hard, push fast, allow complete chest recoil, and minimize interruptions
  in chest compressions. The clinician should only interrupt compressions for ventilation, rhythm
  check, and shock delivery. (See "Basic life support in infants and children", section on 'Chest
  compressions'.)

  Advanced management — Once basic cardiopulmonary resuscitation is established, treatment of
  pulseless arrest requires rapid assessment of rhythm, performance of defibrillation as indicated, and
  pharmacotherapy aimed at increasing coronary artery circulation and restoration of organized
  cardiac conduction (algorithm 5):

         Patients with ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) should
         receive immediate defibrillation. After delivering the shock, five cycles of CPR should be
         performed before checking the rhythm. If the rhythm has not converted with defibrillation, the
         patient should receive a repeated defibrillation at a higher dose. Further unresponsiveness
         requires interposing cardiopulmonary resuscitation with parenteral epinephrine administration
         and antiarrhythmic therapy (eg, amiodarone, lidocaine for VF or VT; magnesium sulfate for
         torsades de pointes). See the algorithm for drug dosing (algorithm 5).

         Patients with asystole or pulseless electrical activity should receive cardiopulmonary
         resuscitation and epinephrine (parenteral administration preferred over endotracheal). See the
         algorithm for drug dosing (algorithm 5).

         During the course of the resuscitation, the clinician should evaluate for underlying causes (H's
         and T's) for the pulseless arrest as indicated on the algorithm (algorithm 5).

     Vascular access — Establishment of reliable vascular access is a critical step in pediatric
  resuscitation. During pulseless arrest, intraosseous cannulation and peripheral venous access should

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  be pursued simultaneously. (See "Vascular (venous) access for pediatric resuscitation and other
  pediatric emergencies" and "Intraosseous cannulation".)

  Resuscitation medications given through a peripheral IV should be followed with a 5 mL flush of
  normal saline to move the drug from the peripheral to the central circulation.

  Many clinicians regard intraosseous cannulation as the preferred initial route of vascular access,
  especially in young infants with pulseless arrest. (See "Intraosseous cannulation".)

  Intraosseous cannulation becomes progressively more difficult as children age because the cortex of
  bone becomes thicker and the tibial bone marrow cavity becomes smaller. However, the
  development of devices, such as spring-loaded single-deployment devices and battery-operated
  handheld drills, has made intraosseous cannulation feasible for patients of all ages, including adults.
  (See "Intraosseous cannulation", section on 'Technique'.)

  Attempts at peripheral and central venous access in the head, neck, and chest should NOT
  interrupt chest compressions. Central lines are more secure than peripheral access and provide
  more rapid onset and higher peak concentration of medications but are NOT required during initial
  resuscitation attempts. If central lines are used, the femoral route is preferred by many. (See
  "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on
  'Femoral vein'.)

      Endotracheal drug administration — Although lipid soluble drugs, such as lidocaine,
  epinephrine, atropine, and naloxone ("LEAN"), may be administered via endotracheal tube (ETT), the
  intravascular route is always preferred. Optimal drug dosing via endotracheal tube is unknown, with
  unpredictable drug absorption leading to lower blood levels when compared with the same dose
  given intravascularly. Several key actions are needed when giving drugs via ETT:

         Increase the epinephrine dose tenfold and the dose of other medications (atropine, lidocaine,
         naloxone) two- to threefold.

         Hold compressions during ETT administration.

         Follow drug administration with 3 to 5 mL of normal saline.

         Provide five positive pressure ventilations after instilling the drug.

     Defibrillation — Defibrillation does not restart the heart; the shock "stuns" the heart by
  depolarizing all of the myocardial cells, hopefully terminating VF and allowing the heart's natural
  pacemaker cells to resume an organized rhythm. After delivering a shock, the caregivers should
  perform five cycles of CPR before checking the rhythm. CPR may be discontinued if a perfusing
  rhythm has been established. (See "Defibrillation and cardioversion in children (including automated
  external defibrillation)", section on 'Methods: Manual defibrillator use'.)

  Biphasic defibrillators have a high first shock efficacy rate for ventricular fibrillation (VF) of short
  duration in adults. This procedure eliminates VF but may not lead to a perfusing rhythm (often the
  patient will be in asystole or PEA) or myocardial ischemia prevents proper cardiac contractility. After
  delivering the shock, chest compressions should resume immediately for five cycles.
  Cardiopulmonary resuscitation is required to maintain blood flow to the heart, coronary circulation,
  and brain until effective cardiac contractility resumes.

  Although manual defibrillators or automated external defibrillators with pediatric attenuating devices
  are preferred for use in infants and children, automated external defibrillators without pediatric
  attenuating devices may be used if they are the only option available. (See "Basic life support in
  infants and children", section on 'Automated external defibrillator'.)

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     Pharmacologic therapy — A detailed discussion of pediatric resuscitation drugs is provided
  separately. (See "Primary drugs in pediatric resuscitation".)

  Epinephrine is the most commonly used medication in children with pulseless arrest. It is classified
  as a catecholamine, vasopressor, and inotrope.

  For pulseless arrest, the IV/IO dosing is 0.01 mg/kg (0.1 mL/kg of the 1:10,000 concentration given
  every three to five minutes; maximum single dose: 1 mg (10 mL)). High dose epinephrine is no
  longer recommended with the exception of endotracheal dosing. When epinephrine is administered
  via ET tube, use 0.1 mg/kg (0.1 mL/kg of the 1:1000 concentration by endotracheal tube every
  three to five minutes). The IV/IO route is always preferred (algorithm 5).

  EARLY POSTRESUSCITATION MANAGEMENT — The early postresuscitation period involves the
  time soon after return of spontaneous circulation or recovery from circulatory or respiratory failure.
  During this time, the clinician must continue to treat the underlying cause for the life-threatening
  event and monitor for common respiratory or circulatory problems that may cause secondary
  morbidity or death [5]:

         Oxygen administration — Once return of spontaneous circulation has been achieved, the
         clinician should titrate inspired oxygen to maintain arterial oxyhemoglobin saturation ≥94
         percent while avoiding hyperoxemia.

         Intubated patients — All intubated children require continued assessment to ensure proper
         endotracheal tube positioning, continuous monitoring of oxygenation (pulse oximetry), and
         ongoing monitoring of ventilation (eg, continuous end-tidal CO2 monitoring, if available, and/or
         intermittent blood gas assessment). Insertion of a gastric tube helps to reduce gastric
         distension.

         The causes of sudden decompensation in a child who has been successfully intubated with an
         artificial airway is described by the mnemonic "DOPE":

             D: Dislodged or displaced endotracheal tube (right mainstem or esophageal location)
             O: Obstructed endotracheal tube (eg, mucous plug, kinked endotracheal tube)
             P: Pneumothorax
             E: Equipment failure (eg, ventilator malfunction, oxygen disconnected or not on)

         Recurrent shock — After fluid resuscitation in a child, circulatory instability may recur as the
         result of ongoing fluid loss, decreased cardiac function, and/or harmful alterations in systemic
         vascular resistance. Goal-directed therapy emphasizes the need to access clinical findings of
         perfusion (eg, capillary refill, urine output), measure central venous pressure, and measure
         central venous oxygen saturation, to determine the best course of action. (See "Initial
         management of shock in children", section on 'Early goal-directed therapy'.)

  If the child is not being treated in a center with pediatric emergency and critical care expertise, the
  child should be stabilized and rapidly transferred for definitive care at a regional pediatric center.
  Critically ill or injured children typically benefit from transport by a team with pediatric expertise and
  advanced pediatric treatment capability, although in some isolated cases (eg, expanding epidural
  hematoma) more rapid transport by an immediately available non-pediatric team may be
  advantageous. (See "Prehospital pediatrics", section on 'Inter-facility transport'.)

  Prior to transfer the physician responsible for the child's care at the transferring hospital should
  speak directly to the physician who will be taking charge of the patient at the receiving hospital. All

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  documentation of care (eg, medical chart, medication administration record, laboratory results,
  copies of ancillary studies (radiographs, ECGs)) should be sent with the patient. (See "Prehospital
  pediatrics", section on 'Inter-facility transport'.)

  RAPID RESPONSE TEAMS — A rapid response team (RRT), also known as a medical emergency
  team, consists of personnel from medical, nursing, and respiratory therapy who have critical care
  training and are available 24 hours per day, seven days a week for evaluation and treatment of
  patients who show signs of clinical deterioration and are located in nonacute care settings (eg,
  medical or surgical inpatient wards). Implementation of a RRT has been promoted as a major
  strategy for improving patient safety in hospitals [8].

  We suggest that pediatric tertiary care centers develop and maintain rapid response teams for the
  prompt assessment and management of hospitalized infants and children who are showing signs of
  clinical deterioration and are located in nonacute care settings. A meta-analysis of five pediatric
  prospective observational studies with a total of 347,618 patient admissions found that
  implementation of a RRT was associated with a significant reduction in deaths when compared to
  historical control periods (103 versus 295 hospital deaths, RR 0.6, 95% CI: 0.5-0.8) [9]. However,
  decreased mortality after implementation of a RRT was not found in all studies.

  A cohort study of 29,294 patient admissions (7257 admissions after institution of a RRT), that was
  included in the metaanalysis previously cited, compared hospital-wide mortality rates and rates of
  respiratory and cardiopulmonary arrests outside of the intensive care unit before and after
  implementation of a RRT in a 264-bed freestanding children’s hospital [10]. Major findings included:

         The mean monthly mortality rate decreased from 1 to 0.8 deaths per 100 discharges (18
         percent decrease, 95% CI: 5-30 percent).

         The mean monthly code rate (respiratory or cardiopulmonary arrest) decreased from 2.5 to
         0.7 codes per 1000 patient admissions (RR 0.3, 95% CI: 0.1-0.7).

         Over 18 months, the RRT was activated 143 times, most commonly for respiratory distress,
         hypotension, hypoxemia, altered mental status, and tachycardia.

         The most common actions by the RRT were respiratory support, fluid resuscitation, airway
         management, and transfer to the intensive care unit.

  Taken together, these findings suggest that the benefit of a RRT, as measured by a decrease in
  hospital mortality, is not consistent across pediatric tertiary care settings. When helpful, a RRT may
  decrease hospital mortality by promptly performing interventions that prevent respiratory or
  cardiopulmonary arrest.

  FAMILY PRESENCE DURING RESUSCITATION — Observational studies indicate that caretakers
  should be given the option of being present during the in-hospital resuscitation of their child [5].
  Key findings include:

         Most parents want the opportunity to remain with their child during resuscitation [5] and
         believe it is their right [11].

         Caretakers present during the resuscitation of a family member frequently reported that their
         presence during the resuscitation was beneficial to the patient [11-13].

         Two-thirds of caretakers present during the resuscitation of a child who died reported that
         their presence helped with their adjustment to the death and the grieving process [13].

         Studies of hospital personnel suggest that the presence of a family member, in most
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         instances, was not stressful to staff and did not negatively impact staff performance [11,12].

  When family members are present during a pediatric resuscitation, a staff member with clinical
  knowledge, empathy, and strong interpersonal skills should be present with them to provide support
  and answer questions.

  In the rare instance that family presence is disruptive to team resuscitation efforts, the family
  members should be respectfully asked to leave.

  SUMMARY — The principle aim for pediatric advanced life support (PALS) is to prevent
  cardiopulmonary failure through early recognition and management of respiratory distress,
  respiratory failure, and shock. (See 'Overview of assessment' above and "Initial assessment and
  stabilization of children with respiratory or circulatory compromise".)

  Respiratory distress and failure — A major goal of pediatric advanced life support is to recognize
  and treat respiratory conditions amenable to simple measures (eg, supplemental oxygen, inhaled
  albuterol) (table 2). The clinician may also have to treat rapidly progressive conditions and
  intervene with advanced therapies to avoid cardiopulmonary arrest in patients with respiratory
  failure. Early detection and treatment improve overall outcome. (See 'Respiratory distress and
  failure' above.)

         Airway — Key steps in basic airway management include (see "Basic airway management in
         children"):

             Provide 100 percent inspired oxygen
             Allow child to assume position of comfort or manually open airway
             Clear airway (suction)
             Insert oropharyngeal airway or nasopharyngeal airway if consciousness impaired

         Breathing — The clinician should assist ventilation manually in patients not responding to
         basic airway maneuvers, monitor oxygenation by pulse oximetry, monitor ventilation by end-
         tidal CO2 if available, and administer medications as needed (albuterol, epinephrine). In
         preparation for intubation, positive pressure ventilation should be initiated with a bag-valve-
         mask to preoxygenate and improve ventilation. (See "Basic airway management in
         children" and "Carbon dioxide monitoring (capnography)".)

         Children who cannot maintain their airway, oxygenation, or ventilatory requirements should
         undergo endotracheal intubation. A rapid overview provides the steps in performing rapid
         sequence intubation (table 3). (See "Emergent endotracheal intubation in children" and "Rapid
         sequence intubation in children".)

  Shock and cardiac arrhythmias

         Proper treatment of shock in children requires the clinician to recognize and eventually
         categorize the type of shock in order to prioritize treatment options (algorithm 1). Early
         treatment of shock may prevent the progression to cardiopulmonary failure (algorithm 2).
         (See "Initial evaluation of shock in children" and "Initial management of shock in children" and
         'Shock' above.)

         Algorithms provide the pediatric advanced life support guidelines for treatment of children with
         tachyarrhythmias (algorithm 4), pulseless arrest (algorithm 5), and symptomatic bradycardia
         (algorithm 3). (See 'Bradyarrhythmias' above and 'Tachyarrhythmias' above and 'Pulseless

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         arrest' above.)

  Postresuscitation care

         The early postresuscitation period includes the time soon after return of spontaneous
         circulation or recovery from circulatory or respiratory failure. During this time, the clinician
         must continue to treat the underlying cause for the life-threatening event and monitor for
         common respiratory or circulatory problems that may cause secondary morbidity or death.

         If the child is not being treated in a center with pediatric emergency and critical care
         expertise, the child should be stabilized and rapidly transferred for definitive care at a regional
         pediatric center.

  Rapid response teams

         We suggest that pediatric tertiary care centers develop and maintain multidisciplinary rapid
         response teams for the prompt assessment and management of hospitalized infants and
         children who are showing signs of clinical deterioration and are located in nonacute care units
         (eg, medical or surgical inpatient wards) (Grade 2B). (See 'Rapid response teams' above.)


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                                                    REFERENCES

    1. ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005
       American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
       Cardiovascular Care. Circulation 2005; 112:IV1.
    2. Ralston, M, Hazinski, MF, Zaritsky, AL, et al. PALS Provider Manual. American Academy of
       Pediatrics, American Heart Association, Dallas, Texas, 2006.
    3. Kleinman ME, de Caen AR, Chameides L, et al. Pediatric basic and advanced life support: 2010
       International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
       Science with Treatment Recommendations. Pediatrics 2010; 126:e1261.
    4. Kleinman ME, de Caen AR, Chameides L, et al. Part 10: Pediatric basic and advanced life
       support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency
       Cardiovascular Care Science With Treatment Recommendations. Circulation 2010; 122:S466.
    5. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support:
       2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
       Cardiovascular Care. Circulation 2010; 122:S876.
    6. Smith BT, Rea TD, Eisenberg MS. Ventricular fibrillation in pediatric cardiac arrest. Acad Emerg
       Med 2006; 13:525.
    7. Samson RA, Nadkarni VM, Meaney PA, et al. Outcomes of in-hospital ventricular fibrillation in
       children. N Engl J Med 2006; 354:2328.
    8. Berwick DM, Calkins DR, McCannon CJ, Hackbarth AD. The 100,000 lives campaign: setting a
       goal and a deadline for improving health care quality. JAMA 2006; 295:324.
    9. Chan PS, Jain R, Nallmothu BK, et al. Rapid Response Teams: A Systematic Review and Meta-
       analysis. Arch Intern Med 2010; 170:18.
   10. Sharek PJ, Parast LM, Leong K, et al. Effect of a rapid response team on hospital-wide
       mortality and code rates outside the ICU in a Children's Hospital. JAMA 2007; 298:2267.
   11. Mangurten J, Scott SH, Guzzetta CE, et al. Effects of family presence during resuscitation and
       invasive procedures in a pediatric emergency department. J Emerg Nurs 2006; 32:225.

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   12. Dudley NC, Hansen KW, Furnival RA, et al. The effect of family presence on the efficiency of
       pediatric trauma resuscitations. Ann Emerg Med 2009; 53:777.
   13. Tinsley C, Hill JB, Shah J, et al. Experience of families during cardiopulmonary resuscitation in a
       pediatric intensive care unit. Pediatrics 2008; 122:e799.




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  GRAPHICS

      Glasgow coma scale and pediatric Glasgow coma scale

             Sign           GCS*                                     PGCS•                         Score
         Eye         Spontaneous           Spontaneous                                             4
         opening
                     To command            To sound                                                3

                     To pain               To pain                                                 2

                     None                  None                                                    1

         Verbal      Oriented              Age-appropriate vocalization, smile, or orientation     5
         response                          to sound, interacts (coos, babbles), follow s objects

                     Confused,             Cries, irritable                                        4
                     disoriented

                     Inappropriate         Cries to pain                                           3
                     words

                     Incomprehensible      Moans to pain                                           2
                     sounds

                     None                  None                                                    1

         Motor       Obeys commands        Spontaneous movements (obeys verbal command)            6
         response
                     Localizes pain        Withdraw s to touch (localizes pain)                    5

                     Withdraw s            Withdraw s to pain                                      4

                     Abnormal flexion      Abnormal flexion to pain (decorticate posture)          3
                     to pain

                     Abnormal              Abnormal extension to pain (decerebrate posture)        2
                     extension to pain

                     None                  None                                                    1

         Best total score                                                                          15

      The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is
      composed of three parameters: best eye response (E), best verbal response (V), and
      best motor response (M). The components of the GCS should be recorded individually;
      for example, E2V3M4 results in a GCS of 9. A score of 13 or higher correlates with mild
      brain injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or
      less represents severe brain injury. The pediatric Glasgow coma scale was validated in
      children 2 years of age or younger. * Data from: Teasdale, G and Jennett, B. Assessment of
      coma and impaired consciousness. A practical scale. Lancet 1974; 2:81.
      • Data from: Holmes, JF, Palchak, MJ, MacFarlane, T, Kuppermann, N. Performance of the pediatric
      Glasgow coma scale in children with blunt head trauma. Acad Emerg Med 2005; 12:814.




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      Causes of acute respiratory distress in children

         Respiratory tract
         Infection
             Epiglottitis
             Retropharyngeal abscess
             Peritonsillar abscess
             C roup
             Tracheitis
             Bronchiolitis
             Pneumonia
         Asthma

         Anaphylaxis

         Foreign body
             Upper airway
             Lower airway
             Esophageal
         Biologic or chemical weapons

         Chest w all/thoracic
             C hest wall deformity (eg, thoracic dystrophy, flail chest)
             Air leak (eg, tension pneumothorax)
             Mass lesion (eg, pulmonary sequestration, malignancy)

         Cardiovascular
         Heart failure

         Cyanotic heart disease

         Pericarditis

         Cardiac tamponade

         Myocarditis

         Nervous system
         Depressed ventilation (from ingestion, injury, or infection)

         Hypotonia (poor pharyngeal tone, ineffective respiratory effort)

         Loss of airway protective reflexes (aspiration)

         Gastrointestinal
         Splinting from abdominal pain

         Abdominal distention

         Aspiration as the result of gastroesophageal reflux

         Metabolic/endocrine
         Acidosis (eg, diabetic ketoacidosis, severe dehydration, sepsis)


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         Hyperthyroidism

         Hypothyroidism

         Hematologic
         Decreased oxygen carrying capacity (eg, severe anemia, methemoglobinemia)

         Trauma
         Blunt or penetrating (eg, pneumothorax, pulmonary contusion)

         Inhalational injury (eg, airw ay burn, smoke inhalation)

      Conditions listed in red are life threatening. Those listed in green are common.




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      Rapid overview of rapid sequence intubation in children

         Preoxygenation
         Begin preoxygenation as soon as the decision to intubate is considered.

         Administer oxygen at the highest concentration available.

         Preparation
         Identify conditions that will affect choice of medications.

         Identify conditions that will predict difficult intubation or bag-mask ventilation.

         Assemble equipment and check for function.

         Develop contingency plan for failed intubation.

         Pretreatment
         Atropine: All children ≤ one year, children <5 years receiving succinycholine, and older
         children receiving a second dose of succinylcholine. Dose: 0.02 mg/kg IV (maximum single
         dose 0.5 mg, minimum 0.1 mg; if no IV access, can be given IM).

         Lidocaine: Optional for increased intracranial pressure. Dose: 1.5 mg/kg IV (maximum dose
         100 mg). Give 2 to 3 minutes before intubation.

         Sedation
         Etomidate: Safe w ith hemodynamic instability, neuroprotective, transient adrenal
         corticosuppression. Do not use in patients w ith focal seizure. Dose: 0.3 mg/kg IV.

         Thiopental: Neuroprotective. Do not use w ith hemodynamic instability. Dose 3 to 5 mg/kg IV.

         Ketamine: Safe w ith hemodynamic instability if patient is not catecholamine depleted. Use
         w ith bronchospasm and septic shock. Do not use w ith increased intracranial pressure. Dose:
         1 to 2 mg/kg IV. (If no IV access, can be given IM dose: 3 to 7 mg/kg).

         Midazolam: Time to clinical effect is longer, inconsistently induces unconsciousness. May
         cause hemodynamic instability at doses required for sedation. Dose: 0.2 to 0.3 mg/kg IV
         (maximum dose 2 mg, onset of effect requires 2 to 3 minutes).

         Paralytic
         Succinycholine: Do not use w ith chronic myopathy or denervating neuromuscular disease; 48
         to 72 hours after burn, crush, or denervating injury; malignant hyperthermia; or pre-exisiting
         hyperkalemia. Dose: infants and young children: 2 mg/kg IV, older children: 1 to 1.5 mg/kg
         IV. (If IV access unobtainable, can be given IM, dose: 3 to 5 mg/kg).

         Rocuronium: Use for children w ith contraindication for succinylcholine. Use w ith extreme
         caution for patients w ho may be difficult to intubate. Suggested dose: 1 mg/kg IV (range 0.6
         to 1.2 mg/kg).

         Protection and positioning
         Maintain manual cervical spine immobilization during intubation in the trauma patient.


         If cervical spine injury is not potentially present, put the patient in the "sniffing position" (ie,
         head forward so that the external auditory canal is anterior to the shoulder and the nose
         and mouth point to the ceiling). Apply cricoid pressure w hen the child is unconscious. Remove
         cricoid pressure if it causes airw ay obstruction or difficulty view ing the larynx.

         If used, maintain cricoid pressure until tracheal tube position is verified.

         Positioning, with placement

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         Confirm tracheal tube placement w ith end-tidal CO2 detection and auscultation.

         Postintubation management
         CXR for tracheal tube placement; provide ongoing sedation, analgesia (eg, fentanyl 1 mcg
         per kilogram), and paralysis.*

      If IV access unobtainable, intraosseous administration of drugs listed is feasible (no
      data for ketamine). * If decompensation after successful intubation use DOPE mnemonic to find
      cause:
      - D: Dislodgement of the tube (right mainstem or esophageal)
      - O: Obstruction of tube
      - P: Pneumothorax
      - E: Equipment failure (ventilator malfunction, oxygen disconnected or not on).




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      Approach to the classification of undifferentiated shock in
      children




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      Approach to the initial management of shock in children




      * For possible cardiogenic shock w ith hypovolemia, give 5 to 10mL/kg, infused over
      10 to 20 minutes. Evaluate target end points and slowly give another 5 to 10 cc/kg
      if there has been improvement or no change.
      • Such as inotropes or vasodilators. For newborns, prostaglandin E1.
      ∆ For patients w ith DKA w ho do not improve with 20 mL/kg, look for another cause
      of shock before administering additional crystalloid. For possible cardiogenic shock,
      slow ly give another 5 to 10 mL/kg if there has been improvement or no change.
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      ◊ Dopamine if normotensive, norepinephrine if hypotensive and vasodilated, and
      epinephrine if hypotensive and vasoconstricted. Adapted from: Carcillo, JA, Fields,
      AI. Clinical practice parameters for hemodynamic support of pediatric and neonatal
      patients in septic shock. Crit Care Med 2002; 30:1365.




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      Pediatric normal vital signs by age

                         Heart rate range            Lower limit of systolic           Respiratory rate
              Age
                          in beats/min                blood pressure (mm                    range
             group
                             (mean)                          Hg)*                       (breaths/min)
         Birth-6       80-180 (140)                60                                 30-60
         months
         (young
         infant)

         6 months-     70-170 (135)                70                                 30-50
         1 year
         (infant)

         1-3 years     90-150 (120)                72-76                              24-40
         (toddler)

         3-5 years     65-135 (110)                76-80                              22-34
         (preschool)

         5-12 years    60-120 (85-100)             80-90                              14-25
         (school
         age)

         12-adult      60-100 (80-85)              90                                 12-20

      * The lower limit of mean arterial pressure (5th percentile at 50th height percentile) in girls and
      boys is estimated by the formula:
      MAP = 1.5 X age(years) + 40. Data from:
      1. Gajewski, KK. Cardiology In: Robertson J, Shilkofski , N. The Harriet Lane Handbook, 17th ed.
      Elsevier Mosby, Philadelphia, PA, 2005, p. 174.
      2. Vital signs in children In: Field, JM, Hazinski, MF, Gilmore, D. Handbook of Emergency Cardiovascular
      Care for Healthcare Providers. American Heart Association, 2006, p. 74.
      3. Silverman, BK. Practical information In: Fleisher, GR, Ludwig, S, Henretig, FM. Textbook of Pediatric
      Emergency Medicine, 5th ed. Lippincott Willams & Wilkins, Philadelphia, PA, 2006, p. 2013.
      4. Wallis, LA, Healy, M, Undy, MB, Maconochie, I. Age related reference ranges for respiration rate and
      heart rate from 4 to 16 years. Arch Dis Child 2005; 90:1117.
      5. Michaud, LJ, Rivara, FP, Grady, MS, et al. Predictors of survival and severity of disability after severe
      brain injury in children. Neurosurgery 1992; 31:254.




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      First degree AV block I




      Electrocardiogram of lead II showing normal sinus rhythm, first
      degree atrioventricular block with a prolonged PR interval of
      0.30 sec, and a QRS complex of normal duration. The tall P
      waves and P wave duration of approximately 0.12 sec suggest
      concurrent right atrial enlargement. Courtesy of Morton Arnsdorf,
      MD.




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      Normal rhythm strip




      Normal rhythm strip in lead II. The PR interval is 0.15 sec and
      the QRS duration is 0.08 sec. Both the P and T waves are
      upright. Courtesy of Morton F Arnsdorf, MD.




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      Mobitz type I (Wenckbach) AV block




      Electrocardiogram showing Mobitz type I (Wenckebach) second
      degree AV block with 5:4 conduction. The characteristics of
      this arrhythmia include: a progressively increasing PR interval
      until a P wave is not conducted (arrow); a progressive
      decrease in the increment in the PR interval; a progressive
      decrease in the RR interval; and the RR interval that includes
      the dropped beat (0.96 sec) is less than twice the RR interval
      between conducted beats (0.53 to 0.57 sec). Courtesy of Morton
      Arnsdorf, MD.




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      Normal rhythm strip




      Normal rhythm strip in lead II. The PR interval is 0.15 sec and
      the QRS duration is 0.08 sec. Both the P and T waves are
      upright. Courtesy of Morton F Arnsdorf, MD.




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      II ECG of mobitz II second degree heart block




      The lead II rhythm strip shows four sinus beats with P wave followed by a
      QRS complex; the fifth P wave is not followed by a QRS complex and
      represents second degree heart block. There is no change in the PR
      interval prior to or after the blocked P wave and thus this is Mobitz II
      second degree heart block. A second episode of second degree heart block
      can be seen after the seventh QRS complex. Reproduced with permission by
      Samuel Levy, MD.




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      Third degree atrioventricular block




      The P waves are completely dissociated from the QRS complexes. The
      QRS complexes are narrow, indicating a junctional escape rhythm. The
      atrial and ventricular rates are stable; the former is faster than the
      latter.




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      Normal rhythm strip




      Normal rhythm strip in lead II. The PR interval is 0.15 sec and
      the QRS duration is 0.08 sec. Both the P and T waves are
      upright. Courtesy of Morton F Arnsdorf, MD.




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      Pediatric bradycardia algorithm (with a pulse and poor
      perfusion): 2010 PALS guidelines




      PALS: pediatric advanced life support; CPR: cardiopulmonary resuscitation; IO:
      intraosseous; IV: intravenous; HR: heart rate; AV: atrioventricular; ABCs: airway,
      breathing, circulation. Reprinted with permission. Pediatric Advanced Life Support:
      2010. American Heart Association Guidelines for Cardiopulmonary Resuscitation and
      Emergency Cardiovascular Care. © 2010 American Heart Association, Inc.




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      AV reentrant tachycardia




      AV reentrant tachycardia breaking to sinus rhythm with Wolff-
      Parkinson-White syndrome.




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      Monomorphic ventricular tachycardia




      Three or more successive ventricular beats are defined as ventricular
      tachycardia (VT). This VT is monomorphic since all of the QRS
      complexes have an identical appearance. Although the P waves are
      not distinct, they can be seen altering the QRS complex and ST-T
      waves in an irregular fashion, indicating the absence of a
      relationship between the P waves and the QRS complexes, ie AV
      dissociation is present.




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      Normal rhythm strip




      Normal rhythm strip in lead II. The PR interval is 0.15 sec and
      the QRS duration is 0.08 sec. Both the P and T waves are
      upright. Courtesy of Morton F Arnsdorf, MD.




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      Drug-induced electrocardiographic abnormalities

         Bradycardia/AV            Supraventricular               Ventricular          QRS and QT
         blockade                  tachycardia                    tachycardia          interval
         Beta blockers             Sympathomimetics               Sympathomimetics
                                                                                       prolongation

                                        Amphetamines                C ocaine           Antidepressants
         Calcium channel
         blockers                       C ocaine                    Amphetamines        Tricyclics

                                        Theophylline                Theophylline        Maprotiline
         Cardiac glycosides
                                        C affeine                 Antidepressants      Antipsychotics
             Digoxin
                                        Methylphenidate             TC As               Phenothiazines
             Digitoxin
             Red squill                 Ephedrine                 Antipsychotics       Antihistamines

             Digitalis lanata           Pseudoephedrine             Phenothiazines      Diphenhydramine

             Digitalis purpurea         Albuterol                 Chlorinated           Astemizole

                                        Dobutamine                hydrocarbons          Terfenadine
             Bufotenin
                                        Epinephrine                 C hloral hydrate   Antiarrhythmics
             Oleander
                                        Dopamine                    Solvents            Quinidine
         Alpha-adrenergic
         agonists                  Anticholinergics               Fluoride              Disopyramide
             Phenylpropanolamine        Antihistamines            Cardiac glycosides    Procainamide
             C lonidine                 TC As                                           Propafenone
                                                                  Potassium
             Imidazolines               Phenothiazines                                  Flecainide, encainide
         Lithium                        C lozapine                                      Amiodarone

         Cholinergics                   Atropine                                        C alcium channel
                                                                                        blockers (rare)
             Organophosphates           Scopolamine
                                                                                        Beta blockers (rare)
             C arbamates           Thyroid hormone
                                                                                       Propoxyphene
         Opioids                   Cellular asphyxiants
                                                                                       Organophosphate
         Sedative-hypnotics        Carbon monoxide                                     insecticides

         Magnesium                 Drug withdraw al                                    Antimicrobials
                                   states
                                                                                        Amantadine
                                                                                        C hloroquine
                                                                                        Erythromycin
                                                                                        Pentamidine
                                                                                        Quinine
                                                                                       Arsenic

                                                                                       Thallium

                                                                                       Fluoride

                                                                                       Citrate

                                                                                       Lithium




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      Pediatric tachycardia algorithm (with a pulse and poor perfusion): 2010
      PALS guidelines




      PALS: pediatric advanced life support; IO: intraosseous; IV: intravenous; ECG:
      electrocardiogram.
      * Vagal manuevers: In infants or young children, place a plastic bag filled w ith ice and cold
      w ater over the face for 15 to 30 seconds or stimulate the rectum with a thermometer. In older
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      children, encourage bearing down (Valsalva maneuver) for 15 to 20 seconds. Carotid massage
      and orbital pressure should not be performed in children. Reprinted with permission. Pediatric
      Advanced Life Support: 2010. American Heart Association Guidelines for Cardiopulmonary
      Resuscitation and Emergency Cardiovascular Care. © 2010 American Heart Association, Inc.




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      Pediatric cardiac arrest algorithm: 2010 PALS guidelines




      PALS: pediatric advanced life support; VF: ventricular fibrillation; VT: ventricular tachycardia;
      PEA: pulseless electrical activity; IO: intraosseous; IV: intravenous; CPR: cardiopulmonary
      resuscitation; ROSC: return of spontaneous circulation. Reprinted with permission. Pediatric
      Advanced Life Support: 2010. American Heart Association Guidelines for Cardiopulmonary
      Resuscitation and Emergency Cardiovascular Care. © 2010 American Heart Association, Inc.
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      Continuous recording during an episode of ventricular fibrillation
      that progresses to asystole




      At the onset of ventricular fibrillation (VF), the QRS complexes are
      regular, widened, and of tall amplitude, suggesting a more organized
      ventricular tachyarrhythmia. Over a brief period of time, the rhythm
      becomes more disorganized with high amplitude fibrillatory waves; this is
      coarse VF. After a longer period of time, the fibrillatory waves become
      fine, culminating in asystole.




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      Torsades de pointes




      This is an atypical, rapid, and bizarre form of ventricular
      tachycardia that is characterized by a continuously changing
      axis of polymorphic QRS morphologies.




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