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• W2484865148 abstract "HomeCirculationVol. 112, No. 24_supplementPart 12: Pediatric Advanced Life Support Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBPart 12: Pediatric Advanced Life Support Originally published28 Nov 2005https://doi.org/10.1161/CIRCULATIONAHA.105.166573Circulation. 2005;112:IV-167–IV-187is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 28, 2005: Previous Version 1 In contrast to adults, sudden cardiac arrest in children is uncommon, and cardiac arrest does not usually result from a primary cardiac cause.1 More often it is the terminal event of progressive respiratory failure or shock, also called an asphyxial arrest.Respiratory FailureRespiratory failure is characterized by inadequate ventilation or oxygenation. Anticipate respiratory failure and possible respiratory arrest if you see any of the following: An increased respiratory rate, particularly with signs of distress (eg, increased effort, nasal flaring, retractions, or grunting)An inadequate respiratory rate, effort, or chest excursion (eg, diminished breath sounds, gasping, and cyanosis), especially if mental status is depressedShockShock results from inadequate blood flow and oxygen delivery to meet tissue metabolic demands. Shock progresses over a continuum of severity, from a compensated to a decompensated state. Attempts to compensate include tachycardia and increased systemic vascular resistance (vasoconstriction) in an effort to maintain cardiac output and blood pressure. Although decompensation can occur rapidly, it is usually preceded by a period of inadequate end-organ perfusion.Signs of compensated shock include TachycardiaCool extremitiesProlonged capillary refill (despite warm ambient temperature)Weak peripheral pulses compared with central pulsesNormal blood pressureAs compensatory mechanisms fail, signs of inadequate end-organ perfusion develop. In addition to the above, these signs include Depressed mental statusDecreased urine outputMetabolic acidosisTachypneaWeak central pulsesSigns of decompensated shock include the signs listed above plus hypotension. In the absence of blood pressure measurement, decompensated shock is indicated by the nondetectable distal pulses with weak central pulses in an infant or child with other signs and symptoms consistent with inadequate tissue oxygen delivery.The most common cause of shock is hypovolemia, one form of which is hemorrhagic shock. Distributive and cardiogenic shock are seen less often.Learn to integrate the signs of shock because no single sign confirms the diagnosis. For example: Capillary refill time alone is not a good indicator of circulatory volume, but a capillary refill time of >2 seconds is a useful indicator of moderate dehydration when combined with a decreased urine output, absent tears, dry mucous membranes, and a generally ill appearance (Class IIb; LOE 32). It is influenced by ambient temperature,3 lighting,4 site, and age.Tachycardia also results from other causes (eg, pain, anxiety, fever).Pulses may be bounding in anaphylactic, neurogenic, and septic shock.In compensated shock, blood pressure remains normal; it is low in decompensated shock. Hypotension is a systolic blood pressure less than the 5th percentile of normal for age, namely: <60 mm Hg in term neonates (0 to 28 days)<70 mm Hg in infants (1 month to 12 months)<70 mm Hg + (2 × age in years) in children 1 to 10 years<90 mm Hg in children ≥10 years of ageAirwayOropharyngeal and Nasopharyngeal AirwaysOropharyngeal and nasopharyngeal airways are adjuncts for maintaining an open airway. Oropharyngeal airways are used in unconscious victims (ie, with no gag reflex). Select the correct size: an oropharyngeal airway that is too small will not keep the tongue from obstructing the pharynx; one that is too large may obstruct the airway.Nasopharyngeal airways will be better tolerated than oral airways by patients who are not deeply unconscious. Small nasopharyngeal tubes (for infants) may be easily obstructed by secretions.Laryngeal Mask AirwayThere is insufficient evidence to recommend for or against the routine use of a laryngeal mask airway (LMA) during cardiac arrest (Class Indeterminate). When endotracheal intubation is not possible, the LMA is an acceptable adjunct for experienced providers (Class IIb; LOE 7),5 but it is associated with a higher incidence of complications in young children.6Breathing: Oxygenation and Assisted VentilationFor information about the role of ventilation during CPR, see Part 11: “Pediatric Basic Life Support.”OxygenThere are no studies comparing various concentrations of oxygen during resuscitation beyond the perinatal period. Use 100% oxygen during resuscitation (Class Indeterminate). Monitor the patient’s oxygen level. When the patient is stable, wean the supplementary oxygen if the oxygen saturation is maintained.Pulse OximetryIf the patient has a perfusing rhythm, monitor oxygen saturation continuously with a pulse oximeter because clinical recognition of hypoxemia is not reliable.7 Pulse oximetry, however, may be unreliable in a patient with poor peripheral perfusion.Bag-Mask VentilationBag-mask ventilation can be as effective as ventilation through an endotracheal tube for short periods and may be safer.8–11 In the prehospital setting ventilate and oxygenate infants and children with a bag-mask device, especially if transport time is short (Class IIa; LOE 18; 310; 49,11). Bag-mask ventilation requires training and periodic retraining on how to select a correct mask size, open the airway, make a tight seal between mask and face, ventilate, and assess effectiveness of ventilation (see Part 11: “Pediatric Basic Life Support”).PrecautionsVictims of cardiac arrest are frequently overventilated during resuscitation.12–14 Excessive ventilation increases intrathoracic pressure and impedes venous return, reducing cardiac output, cerebral blood flow, and coronary perfusion.13 Excessive ventilation also causes air trapping and barotrauma in patients with small-airway obstruction and increases the risk of stomach inflation, regurgitation, and aspiration.Minute ventilation is determined by the tidal volume and ventilation rate. Use only the force and tidal volume needed to make the chest rise visibly. During CPR for the patient with no advanced airway (eg, endotracheal tube, esophageal-tracheal combitube [Combitube], LMA) in place, ventilation rate is determined by the compression-ventilation ratio. Pause after 30 compressions (1 rescuer) or after 15 compressions (2 rescuers) to give 2 ventilations with mouth-to-mouth, mouth-to-mask, or bag-mask techniques. Give each breath over 1 second.If an advanced airway is in place during CPR (eg, endotracheal tube, Combitube, LMA), ventilate at a rate of 8 to 10 times per minute without pausing chest compressions. In the victim with a perfusing rhythm but absent or inadequate respiratory effort, give 12 to 20 breaths per minute. One way to achieve this rate with a ventilating bag is to use the mnemonic “squeeze-release-release” at a normal speaking rate.8,15Two-Person Bag-Mask VentilationA 2-person technique may be more effective than ventilation by a single rescuer if the patient has significant airway obstruction, poor lung compliance, or difficulty in creating a tight mask-to-face seal.16,17 One rescuer uses both hands to maintain an open airway with a jaw thrust and a tight mask-to-face seal while the other compresses the ventilation bag. Both rescuers should observe the victim’s chest to ensure chest rise.Gastric InflationGastric inflation may interfere with effective ventilation18 and cause regurgitation. You can minimize gastric inflation by doing the following: Avoid excessive peak inspiratory pressures (eg, by ventilating slowly and watching chest rise).8 To avoid use of excessive volume, deliver only the volume needed to produce visible chest rise.Apply cricoid pressure. You should do so only in an unresponsive victim. This technique may require an additional (third) rescuer if the cricoid pressure cannot be applied by the rescuer who is securing the bag to the face.19–21 Avoid excessive pressure so as not to obstruct the trachea.22If you intubate the patient, pass a nasogastric or orogastric tube after you intubate because a gastric tube interferes with the gastroesophageal sphincter, allowing possible regurgitation.Ventilation Through an Endotracheal TubeEndotracheal intubation in infants and children requires special training because the pediatric airway anatomy differs from adult airway anatomy. Success and a low complication rate are related to the length of training, supervised experience in the operating room and in the field,23,24 adequate ongoing experience,25 and the use of rapid sequence intubation (RSI).23,26,27Rapid Sequence IntubationTo facilitate emergency intubation and reduce the incidence of complications, skilled, experienced providers may use sedatives, neuromuscular blocking agents, and other medications to rapidly sedate and paralyze the victim.28 Use RSI only if you are trained and have experience using these medications and are proficient in the evaluation and management of the pediatric airway. If you use RSI you must have a secondary plan to manage the airway in the event that you cannot achieve intubation.Cuffed Versus Uncuffed TubesIn the in-hospital setting a cuffed endotracheal tube is as safe as an uncuffed tube for infants beyond the newborn period and in children.29–31 In certain circumstances (eg, poor lung compliance, high airway resistance, or a large glottic air leak) a cuffed tube may be preferable provided that attention is paid to endotracheal tube size, position, and cuff inflation pressure (Class IIa; LOE 230; 329,31). Keep cuff inflation pressure <20 cm H2O.32Endotracheal Tube SizeThe internal diameter of the appropriate endotracheal tube for a child will roughly equal the size of that child’s little finger, but this estimation may be difficult and unreliable.33,34 Several formulas such as the ones below allow estimation of proper endotracheal tube size (ID, internal diameter) for children 1 to 10 years of age, based on the child’s age:Uncuffed endotracheal tube size (mm ID) =(age in years/4) + 4In general, during preparation for intubation using the above formula, providers should have the estimated tube size available, as well as uncuffed endotracheal tubes that have internal diameters that are 0.5 mm smaller and 0.5 mm larger than the size estimated ready at the bedside for use.The formula for estimation of a cuffed endotracheal tube size is as follows30:Cuffed endotracheal tube size (mm ID) = (age in years/4) + 3Endotracheal tube size, however, is more reliably based on a child’s body length. Length-based resuscitation tapes are helpful for children up to approximately 35 kg.35Verification of Endotracheal Tube PlacementThere is a high risk that an endotracheal tube will be misplaced (ie, placed in the esophagus or in the pharynx above the vocal chords), displaced, or become obstructed,8,36 especially when the patient is moved.37 No single confirmation technique, including clinical signs38 or the presence of water vapor in the tube,39 is completely reliable, so providers must use both clinical assessment and confirmatory devices to verify proper tube placement immediately after intubation, during transport, and when the patient is moved (ie, from gurney to bed).Immediately after intubation and again after securing the tube, confirm correct tube position with the following techniques while you provide positive-pressure ventilation with a bag: Look for bilateral chest movement and listen for equal breath sounds over both lung fields, especially over the axillae.Listen for gastric insufflation sounds over the stomach (they should not be present if the tube is in the trachea).38Use a device to evaluate placement. Check for exhaled CO2 (see below) if there is a perfusing rhythm. If the child has a perfusing rhythm and is >20 kg, you may use an esophageal detector device to check for evidence of esophageal placement (see below).Check oxygen saturation with a pulse oximeter. Following hyperoxygenation, the oxyhemoglobin saturation detected by pulse oximetry may not demonstrate a fall indicative of incorrect endotracheal tube position (ie, tube misplacement or displacement) for as long as 3 minutes.40,41If you are still uncertain, perform direct laryngoscopy and look to see if the tube goes between the cords.In hospital settings perform a chest x-ray to verify that the tube is not in the right main bronchus and to identify a high tube position at risk of easy displacement.After intubation secure the tube. There is insufficient evidence to recommend any one method (Class Indeterminate). After you secure the tube, maintain the patient’s head in a neutral position; neck flexion pushes the tube farther into the airway, and extension pulls the tube out of the airway.42,43If an intubated patient’s condition deteriorates, consider the following possibilities (DOPE):Displacement of the tube from the tracheaObstruction of the tubePneumothoraxEquipment failureExhaled or End-Tidal CO2 MonitoringIn infants and children with a perfusing rhythm, use a colorimetric detector or capnography to detect exhaled CO2 to confirm endotracheal tube position in the prehospital and in-hospital settings (Class IIa; LOE 544) and during intrahospital and interhospital transport (Class IIb; LOE 545). A color change or the presence of a capnography waveform confirms tube position in the trachea but does not rule out right main bronchus intubation. During cardiac arrest, if exhaled CO2 is not detected, confirm tube position with direct laryngoscopy (Class IIa; LOE 546–49; 650) because the absence of CO2 may be a reflection of low pulmonary blood flow.You may also detect a low end-tidal CO2 in the following circumstances: If the detector is contaminated with gastric contents or acidic drugs (eg, endotracheally administered epinephrine), you may see a constant color rather than breath-to-breath color change.An intravenous (IV) bolus of epinephrine may transiently reduce pulmonary blood flow and exhaled CO2 below the limits of detection.51Severe airway obstruction (eg, status asthmaticus) and pulmonary edema may impair CO2 elimination.49,52–54Esophageal Detector DevicesThe self-inflating bulb (esophageal detector device) may be considered to confirm endotracheal tube placement in children weighing >20 kg with a perfusing rhythm (Class IIb; LOE 255,56). There is insufficient data to make a recommendation for or against its use in children during cardiac arrest (Class Indeterminate).Transtracheal Catheter VentilationTranstracheal catheter ventilation may be considered for support of oxygenation in the patient with severe airway obstruction if you cannot provide oxygen or ventilation any other way. Try transtracheal ventilation only if you are properly trained and have appropriate equipment.57Suction DevicesA suction device with an adjustable suction regulator should be available. Use a maximum suction force of 80 to 120 mm Hg for suctioning the airway via an endotracheal tube.58 You will need higher suction pressures and large-bore noncollapsible suction tubing as well as semirigid pharyngeal tips to suction the mouth and pharynx.CirculationAdvanced cardiovascular life support techniques are useless without effective circulation, which is supported by good chest compressions during cardiac arrest. Good chest compressions require an adequate compression rate (100 compressions per minute), an adequate compression depth (about one third to one half of the anterior-posterior diameter), full recoil of the chest after each compression, and minimal interruptions in compressions. Unfortunately, good compressions are not always performed for many reasons,14 including rescuer fatigue and long or frequent interruptions to secure the airway, check the heart rhythm, and move the patient.BackboardA firm surface that extends from the shoulders to the waist and across the full width of the bed provides optimal support for effective chest compressions. In ambulances and mobile life support units, use a spine board.59,60CPR Techniques and AdjunctsThere is insufficient data to make a recommendation for or against the use of mechanical devices to compress the sternum, active compression-decompression CPR, interposed abdominal compression CPR, pneumatic antishock garment during resuscitation from cardiac arrest, and open-chest direct heart compression (Class Indeterminate). For further information see Part 6: “CPR Techniques and Devices.”Extracorporeal Membrane OxygenationConsider extracorporeal CPR for in-hospital cardiac arrest refractory to initial resuscitation attempts if the condition leading to cardiac arrest is reversible or amenable to heart transplantation, if excellent conventional CPR has been performed after no more than several minutes of no-flow cardiac arrest (arrest time without CPR), and if the institution is able to rapidly perform extracorporeal membrane oxygenation (Class IIb; LOE 561,62). Long-term survival is possible even after >50 minutes of CPR in selected patients.61,62Cardiovascular MonitoringAttach electrocardiographic (ECG) monitoring leads or defibrillator pads as soon as possible and monitor blood pressure. If the patient has an indwelling arterial catheter, use the waveform to guide your technique in compressing the chest. A minor adjustment of your hand position or depth of compression can significantly improve the waveform.Vascular AccessVascular access is essential for administering medications and drawing blood samples. Venous access can be challenging in infants and children during an emergency, whereas intraosseous (IO) access can be easily achieved. Limit the time you attempt venous access,63 and if you cannot achieve reliable access quickly, establish IO access. In cardiac arrest immediate IO access is recommended if no other IV access is already in place.Intraosseous AccessIO access is a rapid, safe, and effective route for the administration of medications and fluids,64,65 and it may be used for obtaining an initial blood sample during resuscitation (Class IIa; LOE 365,66). You can safely administer epinephrine, adenosine, fluids, blood products,64,66 and catecholamines.67 Onset of action and drug levels achieved are comparable to venous administration.68 You can also obtain blood specimens for type and crossmatch and for chemical and blood gas analysis even during cardiac arrest,69 but acid-base analysis is inaccurate after sodium bicarbonate administration via the IO cannula.70 Use manual pressure or an infusion pump to administer viscous drugs or rapid fluid boluses,71,72 and follow each medication with a saline flush to promote entry into the central circulation.Venous AccessA central intravenous line (IV) provides more secure long-term access, but central drug administration does not achieve higher drug levels or a substantially more rapid response than peripheral administration.73Endotracheal Drug AdministrationAny vascular access, IO or IV, is preferable, but if you cannot establish vascular access, you can give lipid-soluble drugs such as lidocaine, epinephrine, atropine, and naloxone (“LEAN”)74,75 via the endotracheal tube,76 although optimal endotracheal doses are unknown (Table 1). Flush with a minimum of 5 mL normal saline followed by 5 assisted manual ventilations.77 If CPR is in progress, stop chest compressions briefly during administration of medications. Although naloxone and vasopressin may be given by the endotracheal route, there are no human studies to support a specific dose. Non–lipid-soluble drugs (eg, sodium bicarbonate and calcium) may injure the airway and should not be administered via the endotracheal route. TABLE 1. Medications for Pediatric Resuscitation and ArrhythmiasMedicationDoseRemarksIV indicates intravenous; IO, intraosseous; and ET, via endotracheal tube.*Flush with 5 mL of normal saline and follow with 5 ventilations.Adenosine0.1 mg/kg (maximum 6 mg)Monitor ECGRepeat: 0.2 mg/kg (maximum 12 mg)Rapid IV/IO bolusAmiodarone5 mg/kg IV/IO; repeat up to 15 mg/kgMonitor ECG and blood pressureMaximum: 300 mgAdjust administration rate to urgency (give more slowly when perfusing rhythm present)Use caution when administering with other drugs that prolong QT (consider expert consultation)Atropine0.02 mg/kg IV/IOHigher doses may be used with organophosphate poisoning0.03 mg/kg ET*Repeat once if neededMinimum dose: 0.1 mgMaximum single dose: Child 0.5 mg Adolescent 1 mgCalcium chloride (10%)20 mg/kg IV/IO (0.2 mL/kg)SlowlyAdult dose: 5–10 mLEpinephrine0.01 mg/kg (0.1 mL/kg 1:10 000) IV/IOMay repeat q 3–5 min0.1 mg/kg (0.1 mL/kg 1:1000) ET*Maximum dose: 1 mg IV/IO; 10 mg ETGlucose0.5–1 g/kg IV/IOD10W: 5–10 mL/kgD25W: 2–4 mL/kgD50W: 1–2 mL/kgLidocaineBolus: 1 mg/kg IV/IOMaximum dose: 100 mgInfusion: 20–50 μg/kg per minuteET*: 2–3 mgMagnesium sulfate25–50 mg/kg IV/IO over 10–20 min; faster in torsadesMaximum dose: 2gNaloxone<5 y or ≤20 kg: 0.1 mg/kg IV/IO/ET*Use lower doses to reverse respiratory depression associated with therapeutic opioid use (1–15 μg/kg)≥5 y or >20 kg: 2 mg IV/IO/ET*Procainamide15 mg/kg IV/IO over 30–60 minMonitor ECG and blood pressureAdult dose: 20 mg/min IV infusion up to total maximum dose 17 mg/kgUse caution when administering with other drugs that prolong QT (consider expert consultation)Sodium bicarbonate1 mEq/kg per dose IV/IO slowlyAfter adequate ventilationAdministration of resuscitation drugs into the trachea results in lower blood concentrations than the same dose given intravascularly. Furthermore, recent animal studies suggest that the lower epinephrine concentrations achieved when the drug is delivered by the endotracheal route may produce transient β-adrenergic effects. These effects can be detrimental, causing hypotension, lower coronary artery perfusion pressure and flow, and reduced potential for return of spontaneous circulation. Thus, although endotracheal administration of some resuscitation drugs is possible, IV or IO drug administration is preferred because it will provide a more predictable drug delivery and pharmacologic effect.Emergency Fluids and MedicationsEstimating WeightIn the out-of-hospital setting a child’s weight is often unknown, and even experienced personnel may not be able to estimate it accurately.78 Tapes with precalculated doses printed at various patient lengths are helpful and have been clinically validated.35,78,79 Hospitalized patients should have weights and precalculated emergency drug doses recorded and readily available.FluidsUse an isotonic crystalloid solution (eg, lactated Ringer’s solution or normal saline)80,81 to treat shock; there is no benefit in using colloid (eg, albumin) during initial resuscitation.82 Use bolus therapy with a glucose-containing solution to only treat documented hypoglycemia (Class IIb; LOE 283; 684). There is insufficient data to make a recommendation for or against hypertonic saline for shock associated with head injuries or hypovolemia (Class Indeterminate).85,86Medications (See Table 1)AdenosineAdenosine causes a temporary atrioventricular (AV) nodal conduction block and interrupts reentry circuits that involve the AV node. It has a wide safety margin because of its short half-life.A higher dose may be required for peripheral administration than central venous administration.87,88 Based on experimental data89 and a case report,90 adenosine may also be given by IO route. Administer adenosine and follow with a rapid saline flush to promote flow toward the central circulation.AmiodaroneAmiodarone slows AV conduction, prolongs the AV refractory period and QT interval, and slows ventricular conduction (widens the QRS).PrecautionsMonitor blood pressure and administer as slowly as the patient’s clinical condition allows; it should be administered slowly to a patient with a pulse but may be given rapidly to a patient with cardiac arrest or ventricular fibrillation (VF). Amiodarone causes hypotension through its vasodilatory property. The severity of the hypotension is related to the infusion rate and is less common with the aqueous form of amiodarone.91Monitor the ECG because complications may include bradycardia, heart block, and torsades de pointes ventricular tachycardia (VT). Use extreme caution when administering with another drug causing QT prolongation, such as procainamide. Consider obtaining expert consultation. Adverse effects may be long lasting because the half-life is up to 40 days.92AtropineAtropine sulfate is a parasympatholytic drug that accelerates sinus or atrial pacemakers and increases AV conduction.PrecautionsSmall doses of atropine (<0.1 mg) may produce paradoxical bradycardia.93 Larger than recommended doses may be required in special circumstances (eg, organophosphate poisoning94 or exposure to nerve gas agents).CalciumRoutine administration of calcium does not improve outcome of cardiac arrest.95 In critically ill children, calcium chloride may provide greater bioavailability than calcium gluconate.96 Preferably administer calcium chloride via a central venous catheter because of the risk of sclerosis or infiltration with a peripheral venous line.EpinephrineThe α-adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and thus coronary perfusion pressure, a critical determinant of successful resuscitation.97,98PrecautionsAdminister all catecholamines through a secure line, preferably into the central circulation; local ischemia, tissue injury, and ulceration may result from tissue infiltration.Do not mix catecholamines with sodium bicarbonate; alkaline solutions inactivate them.In patients with a perfusing rhythm, epinephrine causes tachycardia and may cause ventricular ectopy, tachyarrhythmias, hypertension, and vasoconstriction.99GlucoseInfants have high glucose requirements and low glycogen stores and develop hypoglycemia when energy requirements rise.100 Check blood glucose concentrations during and after arrest and treat hypoglycemia promptly (Class IIb; LOE 1101; 7 [most extrapolated from neonates and adult ICU studies]).LidocaineLidocaine decreases automaticity and suppresses ventricular arrhythmias102 but is not as effective as amiodarone for improving intermediate outcomes (ie, return of spontaneous circulation or survival to hospital admission) among adult patients with VF refractory to a shock and epinephrine.103 Neither lidocaine nor amiodarone has been shown to improve survival to hospital discharge among patients with VF cardiac arrest.PrecautionsLidocaine toxicity includes myocardial and circulatory depression, drowsiness, disorientation, muscle twitching, and seizures, especially in patients with poor cardiac output and hepatic or renal failure.104,105MagnesiumThere is insufficient evidence to recommend for or against the routine administration of magnesium during cardiac arrest (Class Indeterminate).106–108 Magnesium is indicated for the treatment of documented hypomagnesemia or for torsades de pointes (polymorphic VT associated with long QT interval). Magnesium produces vasodilation and may cause hypotension if administered rapidly.ProcainamideProcainamide prolongs the refractory period of the atria and ventricles and depresses conduction velocity.PrecautionsThere is little clinical data on using procainamide in infants and children.109,110 Infuse procainamide very slowly while you monitor for hypotension, prolongation of the QT interval, and heart block. Stop the infusion if the QRS widens to >50% of baseline or if hypotension develops. Use extreme caution when administering with another drug causing QT prolongation, such as amiodarone. Consider obtaining expert consultation.Sodium BicarbonateThe routine administration of sodium bicarbonate has not been shown to improve outcome of resuscitation (Class Indeterminate). After you have provided effective ventilation and chest compressions and administered epinephrine, you may consider sodium bicarbonate for prolonged cardiac arrest (Class IIb; LOE 6). Sodium bicarbonate administration may be used for treatment of some toxidromes (see “Toxicologic Emergencies,” below) or special resuscitation situations.During cardiac arrest or severe shock, arterial blood gas analysis may not accurately reflect tissue and venous acidosis.111,112PrecautionsExcessive sodium bicarbonate may impair tissue oxygen delivery113; cause hypokalemia, hypocalcemia, hypernatremia, and hyperosmolality114,115; decrease the VF threshold116; and impair cardiac function.VasopressinThere is limited experience with the use of vasopressin in pediatric patients,117 and the results of its use in the treatment of adults with VF cardiac arrest have been inconsistent.118–121 There is insufficient evidence to make a recommendation for or against the routine use of vasopressin during cardiac arrest (Class Indeterminate; LOE 5117; 6121, 7118–120 [extrapolated from adult literature]).Pulseless ArrestIn the text below, box numbers identify the corresponding box in the algorithm (Figure 1.) Download figureDownload PowerPointFigure 1. PALS Pulseless Arrest Algorithm.If a victim becomes unresponsive (Box 1), start CPR immediately (with supplementary oxygen if available) and send for a defibrillator (manual or automated external defibrillator [AED]). Asystole and bradycardia with a wide QRS complex are most common in asphyxial cardiac arrest.1,23 VF and pulseless electrical activity (PEA) are less common122 and more likely to be observed in children with sudden arrest. If you are using an ECG monitor, determine the rhythm (Box 2); if you are using an AED, the device will tell" @default.
• W2484865148 created "2016-08-23" @default.
• W2484865148 creator A5028173083 @default.
• W2484865148 date "2005-12-13" @default.
• W2484865148 modified "2023-10-11" @default.
• W2484865148 title "Part 12: Pediatric Advanced Life Support" @default.
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