pediatric cardiopulmonary resuscitation and stabilization

SYMPOSIUM ON PGIMER PROTOCOLS ON RESPIRATORY EMERGENCIES

Pediatric Cardiopulmonary Resuscitation and Stabilization

Atul Jindal & M. Jayashree & Sunit C. Singhi

Received: 27 January 2011 /Accepted: 8 April 2011 /Published online: 25 May 2011# Dr. K C Chaudhuri Foundation 2011

Abstract Cardiopulmonary arrest refers to cessation ofclinically detectable cardiac activity. In children, it usuallyresults from progression of shock, respiratory failure orcardiac dysrhythmia. Early recognition and timely inter-ventions in above group of patients is the key to preventprogression to cardiac arrest. The goal of resuscitation is tourgently re-establish oxygenation of vital organs byattention to Airway, Breathing and Circulation. Measuresto restore airway patency include positioning, suctioning,continuous positive airway pressure, relieving a foreign-body airway obstruction and, endotracheal intubation,tracheotomy or laryngeal mask airway. Breathing issupported with O2 and if needed, bag-mask ventilation, orendotracheal intubation and ventilation. Patients withabsent or feeble central pulse are given cardiac compres-sions (CPR) at a rate of 100/ min synchronized withventilation. In sudden witnessed collapse, immediatedefibrillation is warranted, followed by CPR and adminis-tration of drugs. In unwitnessed collapse, CPR is performedfor five cycles or 2 min before defibrillation. In patientswith shock, a venous or an intraosseous access is rapidlyestablished to administer 20 ml/kg saline bolus. Supraven-tricular tachycardia is treated with vagal maneuvers andadenosine, if the patient is stable and with synchronizedcardioversion, if unstable. Ventricular tachycardia is treatedwith amiodarone or lidocaine, if stable, and cardioversion ifunstable or if drugs fail. Ventricular fibrillation needsdefibrillation. Aggressive supportive care is needed duringthe post-resuscitation phase. There is no definite marker to

determine futility of CPR. Short duration of arrest, earlyinitiation of CPR, hypothermia as the cause of arrest, andin-hospital arrest have better prognosis.

Keywords Pediatric cardiopulmonary resuscitation . CPR .

Cardiopulmonary arrest . Cardiac arrest . Cardiopulmonaryfailure

Introduction

Cardiac arrest, also referred as cardiopulmonary arrest, isthe cessation of clinically detectable cardiac mechanicalactivity [1]. Clinically, it is characterised by unrespon-siveness, apnea and the absence of detectable centralpulses.

The majority of cardiac arrest in children results fromprogression of shock and respiratory failure (Fig. 1). Thefinal common pathway is respiratory failure and/orcirculatory collapse, resulting in end organ anoxia.Cardiac arrest occurs within 5 min of complete anoxia.The most common causes include respiratory compromisesecondary to upper or lower airway obstruction, intravas-cular volume depletion due to illnesses such as gastroen-teritis, severe sepsis and shock caused by infectiousdiseases such as pneumonia and meningitis, and/ordepressed respiratory drive in neurological conditions.Ten to fifteen percent of cardiac arrests can be due toventricular fibrillation [2]. Only 5% to 12% of childrenwho experience cardiac arrest out of hospital settingsurvive as compared to 27% of those who have had in-hospital cardiac arrest [3]. Early recognition and timelyintervention in seriously ill or injured children is the keyto prevent progression towards cardiac arrest and to savelives.

A. Jindal :M. Jayashree : S. C. Singhi (*)Department of Pediatrics, Advanced Pediatrics Centre,Postgraduate Institute of Medical Education and Research,Chandigarh 160012, Indiae-mail: [email protected]

Indian J Pediatr (September 2011) 78(9):1109–1117DOI 10.1007/s12098-011-0423-z

The goal of resuscitation is to urgently re-establishoxygen and substrate delivery to meet the metabolicdemands of vital organs.

Rapid Cardio Pulmonary Assessment and PhysiologicStatus

The evaluation and management of a seriously ill or injuredchild is done in a stepwise manner using Assess-Categorize-Decide-Act (Details of rapid cardiopulmonaryassessment are given in the protocol on “Initial assessmentand Triage.”) If at any point during the assessment a lifethreatening problem is identified, life saving interventions(resuscitation) are started immediately.

On the basis of rapid cardiopulmonary assessment, thechild is classified as –

& Stable& In respiratory distress or shock& In cardiorespiratory failure

Respiratory Failure

Respiratory failure is defined as inadequate ventilation oroxygenation, or both, that leads to an elevated PaCO2 and /or a decreased PaO2, resulting in acidosis. However,respiratory failure may be functionally characterised as aclinical state that requires intervention to prevent respirato-ry arrest and ultimately cardiac arrest.

Shock

Shock is present when there are signs of poor perfusion. Ablood pressure that is less than the fifth centile for the

child’s age signifies decompensated/hypotensive shock thatrequires rapid, aggressive fluid management.

Cardiopulmonary Failure

Cardiopulmonary failure occurs when there are globaldeficits in ventilation, oxygenation and perfusion.Clinically it manifests with gasping or absent respira-tions, bradycardia or absent pulse, cyanosis and unre-sponsiveness.

Once the child’s physiologic status is determined,management specific to the physiologic status is initiatedusing the ABC format. Frequent sequential assessment,interventions and reassessment as required should beperformed.

Airway Management

Clinical signs of an airway obstruction are breathingdifficulty, inability to speak or breath, poor air entry, or asilent cough. The measures to restore airway patencyinclude positioning, suctioning, relieving a foreign-bodyairway obstruction, and the use of airway adjuncts. Moreadvanced interventions include endotracheal intubation,tracheostomy and cricothyrotomy.

If child is non-responsive, open the airway using headtilt-chin lift, evaluate the airway and check for breathing for5 to 10 s by looking quickly at the chest and abdomenfor signs of movement and listening over the mouth andnose for the movement of air (In trauma patients inwhom a cervical spine injury is suspected, a jaw thrustmaneuver without a head tilt and manual stabilization ofthe head and neck should be done). If there are no signsof respiration, check the oropharynx for foreign objects,then suction the airway of excess secretions. Place thechild in a sniffing position and give rescue breathsrather than waiting for respiratory arrest. It is recom-mended to try “a couple of times” to deliver twoeffective rescue breaths [4]. Rescue breaths should begiven over 1 s, with enough volume to create visiblechest rise. In those who are not breathing, but have apulse, only respirations should be delivered, withoutcompressions. Administer 12 to 20 breaths per min (1breath every 3 to 5 s) for infants and children using bag-valve and mask. During CPR, there is 24% to 33% lessblood flow to the lungs. Therefore, fewer breaths withsmaller volumes are needed for oxygenation and venti-lation [5].

If placing fingers behind the angle of the jaw whilebagging the child is not sufficient to maintain an openairway, either place an oropharyngeal airway or have asecond person bag while the other maintains a patent,

Precipitating conditionsRespiratory Circulatory Sudden cardiac

(Arrhythmias)

Respiratory distress Shock

Respiratory failure

Cardiopulmonary Failure

Cardiac arrest

Fig. 1 Pathway to pediatric cardiac arrest

1110 Indian J Pediatr (September 2011) 78(9):1109–1117

sealed oral airway. The tip of oropharyngeal airway shouldreach approximately to the angle of the jaw.

Airway Foreign Body

In situations of airway foreign bodies; if the child isunresponsive, perform CPR. Do not perform blindfinger sweeps, and “jaw thrust” maneuver. Perform fiveback blows and five chest thrusts for infants, andperform the Heimlich maneuver in older children. Inaddition, suctioning may be required to further open theairway.

Initially, focus on effective bag-valve mask ventilation(BMV) and look for chest expansion. An adequate sealbetween face and mask and mild extension of the neck toopen airway is crucial for adequate chest expansion. Ifchest expansion is insufficient, it is necessary to reassessthe position of the patient, the size of mask andadequacy of seal between mask and face. Duringventilation with bag and mask, gastric distension canoccur, which can compromise ventilation and lead toaspiration of gastric contents.

Endotracheal Intubation

In an unresponsive child, endotracheal intubation shouldbe accomplished as soon as feasible to maximizeventilation and minimize the risk of aspiration. In infantsand children for whom BMV is unsuccessful, endotrachealintubation is needed for securing an airway for airwayrescue or support of ventilation. Insertion of an endotra-cheal tube may cause a prolonged interruption in chestcompressions. Hence, one must weigh the risks and thebenefits.

Endotracheal Tube Type and Sizes Both cuffed anduncuffed tracheal tubes are acceptable for infants andchildren undergoing emergency intubation. A cuffedendotracheal tube is especially useful for those withpoor lung compliance, increased airway resistance, or inthose with a large glottic air leak [5]. Attention must bepaid to tube size, position, and pressures.

During emergency endotracheal intubation cricoid pres-sure can be applied to minimise the risk of aspiration in theunconscious patient. However, there are no data to supportthis assumption [6]. If cricoid pressure impedes ventilationor interferes with the speed or ease of emergencyintubations, it should be discontinued.

In infants ≥3.5 kg and <1 year of age, if a cuffed trachealtube is used it is reasonable to use a tube with an internaldiameter of 3.0 mm. In children between 1 and 2 years ofage, if a cuffed tracheal tube is used, use a tube with aninternal diameter of 3.5 mm [6].For children 2 to 10 years

of age, the endotracheal size (mm, internal diameter) can becalculated by the following formulas [6]:

Cuffed endotracheal tube size ¼ age in years=4ð Þ þ 3:5

Uncuffed endotracheal tube size ¼ age in years=4ð Þ þ 4

Once placed, the endotracheal tube cuff pressureshould be maintained at less than 20–25 cm H2O [6]. Itis important to repeatedly verify endotracheal tubeplacement after the tube is inserted, during transport, andafter the movement of the patient. Verification of tubeplacement should be done by clinical assessment (equalchest size and auscultation of breath sounds on both sides)and if available, by capnography. However, use ofcapnography is limited to those patients exhibiting aperfusing rhythm weighing more than 2 kg [7]. No singleassessment method accurately or consistently confirmstracheal tube placement, despite the common practice ofrelying on auscultation.

Cricothyroidotomy or tracheostomy are rarely requiredin ER. Complications from these procedures are common,and ventilation can almost always be maintained with bagand mask until intubation can be accomplished.

Breathing: Ventilatory Management

Tachypnea, irregular or increased respiratory effort mani-festing as nasal flaring, retractions or accessory muscle use,inadequate and unequal chest wall excursion and dimin-ished air movement on the auscultation are signs ofbreathing inadequacy/difficulty. Retractions plus stridorindicate upper airway obstruction. Retractions plus wheezeindicate lower airway obstruction. Retraction plus grunt/laboured breathing indicate parenchymal lung disease.

O2 saturation ≥94% at room air suggests adequateoxygenation. Additional interventions are required if O2

saturation is <92% in a child receiving 100% O2 bynonrebreathing mask.

Bag and mask ventilation should be administered handin hand with chest compressions, at a rate of 8 to 10 permin. There are insufficient data to recommend an optimaltidal volume and respiratory rate during Bag and maskventilation [6]. There is also insufficient evidence torecommend any specific inspired oxygen concentration forventilation during resuscitation. Once circulation is re-stored, titrate inspired O2 to limit hyperoxemia.

Avoid hyperventilation, as it can be harmful Increasedrespiratory rates cause an increased intrathoracic pressure,thereby decreasing venous return and coronary perfusionpressure. Hyperventilation reduces CO2 and causes alkalosis,which can lead to decreased cerebral perfusion and decreased

Indian J Pediatr (September 2011) 78(9):1109–1117 1111

tissue oxygen delivery respectively. This has been shown todecrease survival rates [8]. Hyperventilation is a usefulstrategy only in presence of increased intracranial pressurewith an immediate risk of transtentorial herniation.

Airway and ventilation should be repeatedly reassessedthroughout resuscitation. In addition, the oxygen deliverysystem should be double-checked to assure that maximumoxygen is being delivered to the patient.

Management of Circulation

The assessment of cardiovascular function includes heartrate and rhythm, blood pressure, peripheral and centralpulses, capillary refill time, and skin color and temperature.The heart rhythm can initially be determined as beingregular or irregular. To further define the rhythm distur-bance, connect patients with absent, too fast or too slow,and irregular pulse to a cardiac monitor. The importantdysrhythmias to recognize are ventricular fibrillation,ventricular tachycardia, pulseless electrical activity (PEA),asystole, and supraventricular tachycardia. Because cardiacarrest in children is predominately caused by anoxia, mostchildren present with bradycardia or asystole. Only about10% of children with cardiac arrest present with ventricularfibrillation and commonly have ventricular rhythms withcardiac arrest.

The management modalities to restore circulation andcardiovascular function include cardiac compressions,defibrillation, obtaining a venous access, and administrationof fluid bolus for shock and drugs for rhythm disturbances.

Chest Compression

In an unresponsive child with no visible sign of life, afterdelivery of rescue breaths, attempt to feel carotid orbrachial pulse for 5 to 10 s. If pulse is not felt definitelywithin 10 s, high quality cardiopulmonary resuscitation(CPR) should be started. Also begin chest compression(CPR) in following situations:

& In an unresponsive child who is not breathing normally,and a pulse cannot be palpated within 10 s.

& A weak central pulse: It is a worrisome sign requiringvery rapid intervention to prevent cardiac arrest.

& Bradycardia (heart rate of less than 60 beats per min)coupled with signs of low cardiac output. Bradycardiais often a terminal sign; therefore, do not wait forpulseless arrest to start chest compression.

Effective chest compressions improve survival byproviding blood flow to vital organs during resuscitation.

Compression Rate Compressions should be performed at arate of 100 per min for all ages, except newborns. Thecompression to ventilation ratio is 30:2 for single rescuers,while the ratio is 15:2 for two-rescuers. It allows forsufficient time for adequate chest recoil, to allow foradequate cardiac filling and venous return [9].

Compression Technique Place heel of one hand in thecentre of chest between nipples and other hand on top ofthe first hand to start effective compression. In infantscompression should be delivered just below the nippleline. For infants, use two thumbs pressing on thesternum, with the hands encircling the chest. Deliverchest compressions that depress the chest of the infantand child by one third to one half the anterior posteriordimension or approximately 4 cm (1.5 in.) in infants and5 cm (2 in.) in children.

American Heart Association recommends “push hard,push fast, minimise interruptions; allow full chest recoil”.When performing chest compressions, rescuers should bechanged after five cycles of CPR, or 2 min to decreaserescuer fatigue. This switch should be performed in lessthan 5 s to minimize interruptions in CPR [10].

Interruptions in compressions should be limited to lessthan 10 s for interventions such as placing an advancedairway or defibrillation. Interruptions in compressions haveshown to decrease the rate of return to spontaneouscirculation. Rhythm checks should be performed every2 min, or five cycles of CPR. Once an advanced airway isin place, compressions and breaths should be performedcontinuously without interruption.

Venous Access

A vascular access is needed for the administration of fluidsand all drugs. If a peripheral venous access cannot beachieved in three attempts or 90 s, intraosseous accessshould be attempted. If neither a bone marrow nor aspecifically designed intraosseous needle is available, atwo-inch, 18 to 20 gauge spinal needle can be used. Thepreferred location is on the flat, medial surface of theproximal tibial shaft 1 to 2 cm below the tibial tuberosity.Alternately, especially in older children or adolescents, aneedle can be placed in the medial surface of the tibiaproximal to the medial malleolus. All resuscitation drugsand fluids can be delivered rapidly and safely via this route(Table 1).

If intraosseous access is unsuccessful, central venousaccess (preferably femoral) should be obtained. If vascularaccess is unavailable, lipophilic drugs may be administeredat higher doses through the endotracheal tube. These drugsinclude “LEAN”: lidocaine, epinephrine, atropine, andnaloxone [11].


Defibrillation

In situations of sudden witnessed collapse, immediatedefibrillation is warranted, followed by CPR, and drugadministration. If the collapse is unwitnessed, CPR shouldbe performed for five cycles or 2 min before the use of thedefibrillator. CPR should be provided with minimalinterruption until the electrode pads are attached. CPRprovides some blood flow, delivering oxygen and substrateto the heart muscle, thereby making it more likely to abortventricular fibrillation.

Administer a single shock at a dose of 2–4 J/kg,followed by immediate CPR. In at least 90% of cases,ventricular fibrillation is eliminated by the first shock [12].The cases in which the first shock does not terminateventricular fibrillation, CPR is beneficial immediately postdefibrillation (Fig. 2). This ‘primes’ the heart for the nextdefibrillation attempt. In unwitnessed collapse giving CPRbefore defibrillation increased survival rates from 4% to22% [13]. If ventricular fibrillation persists, then administera second shock of 4 J/kg. Higher subsequent energy dosesmay be safe and effective [6]. This should be followed byimmediate resumption of CPR for five cycles. During thiscycle, give first dose of epinephrine soon after starting theCPR. If ventricular fibrillation continues during the rhythmcheck, give a third shock of 4 J/kg; this should be followed

by resumption of CPR and administration of an antiar-rhythmic drug. Remember success of electric shock isimproved if effective chest compressions are provided for2 min before defibrillation, and CPR is resumed immedi-ately after the first shock and continued for five cycles(about 2 min) before the next rhythm check.

In cases of asystole or pulseless electrical activity (PEA)initiate immediate CPR. More specifically, the treatment ofeach rhythm disturbance can be classified according to theTachycardia Algorithm (Fig. 3). The presence or absence ofpulse determines which arm of the algorithm to initiate forunstable rythm (eg. polymorphic ventricular tachycardia)use high energy unsynchronized shocks rather than syn-chronized shocks. Low-energy unsynchronized shocks havea high likelihood of provoking ventricular fibrillation [4].

Drugs During CPR

Drug delivery should not interrupt CPR. The timing of drugdelivery is less important than continued chest compressions.The standard recommended dose of epinephrine duringcardiac arrest is 0.01 mg/kg IV or intraosseous (maximumsingle dose is 1 mg); it correlates to 0.1 mL/kg. It may begiven via the endotracheal tube when IV/IO access is notavailable (dose 0.1 mg/kg). Epinephrine increases coronaryperfusion pressure and cerebral blood flow. High-dose

Table 1 Drugs commonly used during resuscitation and their doses

Drug Dose Concentration Comment

Atropine 0.02 mg/kg/dose Range 0.1 mg to 1.2 mg/ml Recommended minimum dose 0.1 mg, maximumdose 0.5 mg for a child

Adenosine 0.1 mg/kg IV/IO 3 mg/ml Rapid bolus using two syringe technique

Calcium chloride 20 mg/kg/dose 100 mg/ml (10%) Use with central venous access

Dopamine 2–20 μg/kg/min 40, 80 and 160 mg/ml Titrate to desired effect

Epinephrine 0.01 mg/kg/dose 0.1 mg/ml (1:10,000) High dose not recommended

Epinephrine (infusion) 0.1–1.0 μg/kg/min Titrate to desired effect

Glucose 0.5 to 1 g/kg/dose D5W (0.05 g/ml) More important in neonatesD10W (0.1 g/ml)

D25W (0.25 g/ml)

D50W (0.5 g/ml)

Lidocaine 1 mg/kg/dose 10 & 20 mg/mI Give bolus undiluted over 2–4 min

Lidocaine infusion 20–50 μg/kg/min (1 &2%)

Sodium bicarbonate 1 mEq/kg/dose 0.5–1 mEq/ml (4.2 & 8.4%) Use only if ventilation is established

Amiodarone 5 mg/kg over 20-mins

CPR Rhythm check Pulseless arrest VF/VT

Defibrillation2-4 J/kg

CPR5cycles(2 mins)

Drugs

Fig. 2 Sequence of resuscitation, in pulseless arrest with ventricular fibrillation (VF) and ventricular tachycardia (VT)


epinephrine (1:1000 concentration intravenous) is not rec-ommended in any age group, and is actually associated witha worse outcome, especially in cases of asphyxia [14].Amiodarone is the preferred drug for treatment for suddenpulseless arrest, since it is more effective. If amiodarone isunavailable, lidocaine may be used [15].

Epinephrine (Adrenaline) is also used for children withbradycardia and poor perfusion that is unresponsive toventilation and oxygenation. It is reasonable to administeratropine for bradycardia caused by increased vagal tone(near-drowning, during endotracheal suction/ intubation) orcholinergic drug toxicity.

Glucose should not be administered during CPR, exceptwhen hypoglycemia is documented. Hyperglycemia isassociated with poor prognosis.

Vasopressin is still a controversial drug in pediatric CPR.Routine administration of sodium bicarbonate is not

recommended while routine use of calcium for infants andchildren with cardiopulmonary arrest is not recommendedin the absence of hypocalcemia, calcium channel blockeroverdose, hypermagnesemia, or hyperkalemia [6].

Shock

When a child is assessed to be in shock, Oxygenadministration and monitoring are followed by establish-ment of a venous/intraosseous access. Isotonic crystalloid(normal saline or lactated ringer) solutions should be givenas rapid fluid boluses of 20 ml/kg up to 60–80 ml/kg. Thereis insufficient evidence to justify superiority of any specificisotonic crystalloid over others.

The optimal timing for intubation of children in shockremains unclear, although reports suggest potential benefi-cial effects of early intubation before signs of respiratoryfailure develop.

Blood transfusion may be required in shock secondary totraumatic blood loss in presence of hypotension or ifperfusion parameters do not normalise after a total of 40–60 ml/kg of fluid.

Inotropic agents should be considered if septic orcardiogenic shock persists after intravascular volume hasbeen repleted. Dopamine is usually the inotrope of firstchoice. However, selection of an inotrope or vasopressor toimprove hemodynamics should be tailored to each patient’sphysiology and adjusted as clinical status changes.

Stress dose corticosteroids may be considered in childrenwith septic shock unresponsive to fluids and requiringvasoactive support. However, there is insufficient evidenceto support or refute the routine use of stress dose or lowdose hydrocortisone and /or other corticosteroids in infantsand children with septic shock [6].

Titration of superior vena caval oxygen saturation ≥70%may be beneficial for infants and children with fluidrefractory septic shock.

Dysrrhythmias

Primary dysrhythmias are uncommon in the pediatricpopulation. They typically occur secondary to hypoxemiaor shock rather than being the cause of shock orcardiopulmonary failure. Supraventricular tachycardiaoccurs as a primary dysrhythmia, particularly in the firstyear of life. Algorithm for management of rhythmdisturbances in Emergency room based on initial pulsecheck is given in Fig. 4.

Supraventricular Tachycardia For the treatment of supra-ventricular tachycardia in the hemodynamically stablepatient (palpable pulse and normal arterial pressure), vagalmaneuvers may be used initially (for example: ice on theface), but, in the event of treatment failure, the drug ofchoice is adenosine at a dose of 0.1 mg/kg, or 0.2 mg/kg incases refractory to the initial dose. Adenosine has a shorthalf-life and should be injected rapidly. The most effectivemeans of administration is to use two syringes at the same

A. Ventricular Fibrillation

B. Ventricular Tachycardia

C. Supra ventricular tachycardia

D. Torsades de Pointes

Fig. 3 Important dysrhythmias to be recognized in ER: ventricularfibrillation, ventricular tachycardia, supraventricular tachycardia andTorsades de Pointes


time, one containing the drug and the other with a salinesolution push.

Amiodarone is also useful in treating pediatric supra-ventricular tachycardia, and can be used when adenosinehas failed to convert to, or to maintain a normal sinusrhythm, in hemodynamically stable patients.

Hemodynamically unstable patients with supraventricu-lar tachycardia should receive electrical cardioversion asquickly as possible. Remember to set the defibrillator tosynchronized mode! The dose is 0.5–1 J/kg on the firstattempt and 2 J/kg in subsequent attempts.

Hemodynamically stable patients with ventricular tachy-cardia can be treated with amiodarone or Lidocaine.

In Patients with VF or without a pulse CPR should bestarted immediately while awaiting a defibrillator, asdefibrillation is the treatment of choice.

Postresuscitative Care

& Avoid hyperventilation and hyperoxemia& Maintain a normal body temperature. It is important to

avoid hyperthermia, especially in hypoxic-ischemic

events and very low-weight infants. Recent evidenceis insufficient to recommend the routine use of systemicor selective cerebral hypothermia after resuscitation.

& Start vasoactive drugs to maintain blood pressure(Table 1); epinephrine is preferred drug in post arrestsituations. Recent studies recognize the probable benefitof vasoactive medications, including ionodilators (inam-rinone, milrinone) to treat post-resuscitation myocardialdepression. The level of arterial blood pressure duringthe first 2 h after resuscitation was directly correlatedwith good functional neurological recovery, whereasarterial hypertension in the first 5 min after return ofspontaneous circulation did not influence outcome [16].

& Maintain blood glucose. The unnecessary administra-tion of glucose during or soon after CPR may impactnegatively on prognosis. Therefore, the objective is tomaintain normoglycemia [6].

& When sudden unexplained cardiac arrest occurs inchildren and young adults, a complete past medicaland family history (including a history of syncopalepisodes, seizures, unexplained accidents, or suddendeath) should be obtained and any available previousECGs should be reviewed.

Pulse Check

No Pulse Pulse present

VFVTTorsades

PEAAsystole

SVT VT

Defibrillation 2-4 J/kg

Epinephrine q 3-5min. IV/IO 0.01mg/kg(1:10000)

Defibrillation 4J/kg

Amiodarone IV/IO 5mg/kgOr Lidocaine IV/IO1mg/kgOr Magnesium(torsades)IV/IO 25-50 mg/kg

Defibrillation 4J/kg

Epinephrine q 3-5 min.

IV/IO 0.01mg/kg(1:10000)Or Atropine IV/IO .01mg/kg(upto 3 doses)

Epinephrine q 3-5 min.

IV/IO 0.01mg/kg(1:10000)

Identify underlying causes of PE

6H and 5T

Cardioversion 0.5-1J/kg

Cardioversion 0.5-1J/kg

Vagal maneuvers

AdenosineIV/IO 0.1mg/kg(max 6 mg)

AdenosineIV/IO 0.2mg/kg(max 12 mg)

Consider alternative: Amiodarone

Cardioversion0.5-1J/kg

Amiodarone5mg/kg Iv over 30 min.Or procainamide15 mg/kg IV over 10-15 min

Cardioversion2J/kg

CPR CPR

Start CPRAttach a monitor

Attach a monitor

Fig. 4 Algorithm for management of rhythm disturbances inEmergency room based on initial pulse check . 6 H.s are Hypovole-mia, Hypoxia, Hydrogen ion (Acidosis), Hypo-/hyperkalemia,

Hypoglycaemia, Hypothermia. 5 T.s are Toxins, Temponade, cardiac,Tension pneumothorax, Thrombosis (coronary or pulmonary),Trauma (hypovolemia)


Setting Up a Team

The presentation of a young child in cardiopulmonary arrestis anxiety provoking and often results in a chaoticresuscitation. Optimal performance is derived from havinga PALS-trained team with at least five members having pre-assigned specific roles. The most experienced personshould take over as team leader and assign individualsroles to manage the airway, perform chest compressions,establish venous access, place and maintain monitors,assess vital signs, draw up medications, and apply cardiacdefibrillation.

Prognosis and Decision to Terminate CPR

There is no clear indicator suggesting a point after whichcontinued efforts of CPR are futile. There are certainindicators that suggest a likelihood of better prognosis,including: short duration of cardiorespiratory arrest, earlyinitiation of CPR, hypothermia as the cause of cardio-respiratory arrest and cardio-respiratory arrest in a hospital.Duration of resuscitation is directly related to neurologicalprognosis, i.e. the longer the CPR lasts the greater the riskof neurological damage. New evidence suggests that thelength of resuscitation is not an adequate prognosticindicator of survival. Intact survival has been reported,even in those cases with prolonged resuscitation and twodoses of epinephrine have been administered [17]. Thereare isolated reports of prolonged cardiorespiratory arrestwith minimal sequelae, in particular when good CPR isperformed. For these reasons there is no consistentguideline as to when to stop resuscitation [17].

Key Points

& In a patient in cardiopulmonary arrest establish airway;give 2 rescue breaths, if no /poor breathing effort

& Perform effective CPR, push hard and fast at 100compression/min limiting interruptions

& Start effective bag valve—mask ventilation with oxygen& Continue with a compression:ventilation ratio 30:2

(lone rescuer), 15:2(2 rescuers)& Compress at least one third of the anteroposterior

dimension of the chest during CPR& Consider and perform endotracheal intubation if BMV

is unsuccessful. Both cuffed and uncuffed tubes areacceptable. The safety and value of using cricoidpressure during emergency intubation are not clear

& Once advanced airway is in place: Bag ventilationshould be administered at a rate of 8 to 10 per minsimultaneously with chest compressions

& Avoid hyperventilation& Once spontaneous circulation is restored, inspired

oxygen concentration should be titrated to limit the riskof hyperoxemia

& Defibrillation : single shock 2–4 J/kg, followed byimmediate resumption of CPR. Rhythm check after fivecycles or 2 min, for subsequent defibrillation shockhigher than 4 J/kg may be safe and effective

& IV/IO route is preferable to endotracheal tube for drugadministration

& Amiodarone is the drug of choice for pulseless arrest& Bundled approach to management of pediatric septic

shock: O2, IV access and fluid bolus

References

1. Ralston M, Hazinski M, Zaritsky A, et al. Pediatric assessment.Pediatric advanced life support, provider manual. Dallas: Amer-ican Heart Association; 2006. p. 1–32.

2. Donoghue AJ, Nadkarni V, Berg RA, et al. Out-of-hospitalpediatric cardiac arrest: an epidemiologic review and assess-ment of current knowledge. Ann Emerg Med. 2005;46:512–22.

3. Nadkarni VM, Larkin GL, Peberdy MA, et al. First documentedrhythm and clinical outcome from in-hospital cardiac arrestamong children and adults. JAMA. 2006;295:50–7.

4. American Heart Association. Guidelines for cardio-pulmonaryresuscitation and emergency cardiovascular care. Part 12: pediatricadvanced life support. Circulation. 2005;112:167–87.

5. Newth C, Rachman B, Patel N, et al. The use of cuffed versusuncuffed endotracheal tubes in pediatric intensive care. J Pediatr.2004;144:333–7.

6. de Caen AR, Kleinman ME, Chameides L, et al. Part 10:paediatric basic and advanced life support: 2010 internationalconsensus on cardiopulmonary resuscitation and emergencycardiovascular care science with treatment recommendations.Resuscitation. 2010;81S:e213–59.

7. Bhende M, Thompson A, Orr R. Utility of an end-tidal carbondioxide detector during stabilization and transport of critically illchildren. Pediatrics. 1992;89:1042–4.

8. Aufderheide T, Lurie K. Death by hyperventilation: a commonand life-threatening problem during cardiopulmonary resuscita-tion. Crit Care Med. 2004;32:S345–51.

9. Aufderheide T, Pirrallo R, Yannopoulos D, et al. Incompletechest wall decompression: a clinical evaluation of CPR perfor-mance by EMS personnel and assessment of alternative manualchest compression-decompression techniques. Resuscitation.2005;64:355–62.

10. Ashton A, McCluskey A, Gwinnutt C, et al. Effect ofrescuer fatigue on performance of continuous externalchest compressions over 3 min. Resuscitation. 2002;55:151–5.

11. Johnston C. Endotracheal drug delivery. Pediatr Emerg Care.1992;8:94–7.

12. Martens P, Russell J, Wolcke B, et al. Optimal response to cardiacarrest study: defibrillation waveform effects. Resuscitation.2001;49:233–43.

13. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality ofcardiopulmonary resuscitation during out-of-hospital cardiacarrest. JAMA. 2005;293:299–304.


14. Perondi M, Reis A, Paiva E, et al. A comparison of high-dose andstandard-dose epinephrine in children with cardiac arrest. N Engl JMed. 2004;350:1708–9.

15. Dorian P, Cass D, Schwartz B, et al. Amiodarone as comparedwith lidocaine for shock-resistant ventricular fibrillation. N Engl JMed. 2002;346:884–90.

16. Sterz F, Zeiner A, Kurkciyan I, et al. Mild resuscitativehypothermia and outcome after cardiopulmonary resuscitation. JNeurosurg Anesthesiol. 1996;8:88–96.

17. Lopez-Herce J, Garcia C, Dominguez P, et al. Characteristics andoutcome of cardiorespiratory arrest in children. Resuscitation.2004;63:311–20.


pediatric cardiopulmonary resuscitation and stabilization

Documents