History

Fact Explanation
History of respiratory disease In infants and children cardiac arrest does not usually occur from a primary cardiac cause. Often it occur as the end result of progressive respiratory failure or shock. Patients with cardiomyopathy can present with symptoms as exercise-induced bronchospasm. [1],[2],[3].
History of cardiac disease Some underlying cardiac disorders associated with pediatric cardiac arrest. In general, causes can be considered structural, functional (expected to be identified with echocardiography or at autopsy) or primary electrical disorders (most commonly associated with structurally and functionally normal hearts).[1],[2],[3].
Dizziness Due to the arrhythmias cerebral perfusion becomes impaired. [1],[2],[3].
Chest pain Chest pain is almost never present in patients with primary electrical disorders but is more likely in patients with cardiomyopathies, congenital coronary artery abnormalities, or aortic disease. (eg, dissection or rupture associated with Marfan syndrome) [1],[2],[3].
Syncope In arrhythmias due to the impaired cerebral perfusion syncopal attacks occur. [1],[2],[3].
Palpitations In arrhythmias heart rate may increased to a level that patient producing a pounding or flipping sensation. [1],[2],[3].
Dyspnea Due to the incoordinated heart muscle contraction cardiac output is impaired. Increase in respiration is a compensatory mechanism. [1],[2],[3].
Family history of premature, unexpected sudden death Studies have reported cardiac symptoms in 27% of surviving relatives, with a 22% incidence of unexpected premature sudden death in addition to the proband in any relative and a 6% incidence of sudden death in a first-degree relative. [1],[2],[3].
References
  1. KLEINMAN M. E., CHAMEIDES L., SCHEXNAYDER S. M., SAMSON R. A., HAZINSKI M. F., ATKINS D. L., BERG M. D., DE CAEN A. R., FINK E. L., FREID E. B., HICKEY R. W., MARINO B. S., NADKARNI V. M., PROCTOR L. T., QURESHI F. A., SARTORELLI K., TOPJIAN A., VAN DER JAGT E. W., ZARITSKY A. L.. Part 14: Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation [online] December, 122(18_suppl_3):S876-S908 [viewed 04 August 2014] Available from: doi:10.1161/​CIRCULATIONAHA.110.971101
  2. TRESS EE, KOCHANEK PM, SALADINO RA, MANOLE MD. Cardiac arrest in children J Emerg Trauma Shock [online] 2010, 3(3):267-272 [viewed 04 August 2014] Available from: doi:10.4103/0974-2700.66528
  3. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144

Examination

Fact Explanation
Pulse examination Pulse can be irregularly irregular with a increased rate.
Tachypnea In asphyxial arrest due to systemic hypoxemia, hypercapnia and acidosis as a compensatory mechanism respiratory rate becomes increased.
References
  1. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144
  2. KLEINMAN M. E., CHAMEIDES L., SCHEXNAYDER S. M., SAMSON R. A., HAZINSKI M. F., ATKINS D. L., BERG M. D., DE CAEN A. R., FINK E. L., FREID E. B., HICKEY R. W., MARINO B. S., NADKARNI V. M., PROCTOR L. T., QURESHI F. A., SARTORELLI K., TOPJIAN A., VAN DER JAGT E. W., ZARITSKY A. L.. Part 14: Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation [online] December, 122(18_suppl_3):S876-S908 [viewed 04 August 2014] Available from: doi:10.1161/​CIRCULATIONAHA.110.971101
  3. ARNESTAD M., CROTTI L., ROGNUM T. O., INSOLIA R., PEDRAZZINI M., FERRANDI C., VEGE A., WANG D. W., RHODES T. E., GEORGE A. L., SCHWARTZ P. J.. Prevalence of Long-QT Syndrome Gene Variants in Sudden Infant Death Syndrome. Circulation [online] 2007 January, 115(3):361-367 [viewed 04 August 2014] Available from: doi:10.1161/​CIRCULATIONAHA.106.658021

Differential Diagnoses

Fact Explanation
Hypertrophic cardiomyopathy This can present with dizziness/palpitation/ syncope and carries a high incidence of sudden death. There is inappropriate myocardial hypertrophy which is and often asymmetrica. This occurs in the absence of an obvious hypertrophic stimulus. [1]
Coronary artery anomalies Coronary artery anomalies are uncommon findings but can be significant. Clinical presentation depends on the specific anomaly. Most are benign and clinically insignificant, but some are significant and may cause heart failure and even death.[2]
Marfan’s syndrome Marfan syndrome is caused by a hereditary genetic defect of connective tissue. It has an autosomal dominant mode of transmission. In this syndrome dilatation of the ascending aorta can occur in cardiovascular system. [3]
Congenital heart disease Children with congenital heart disease have significant mortality, especially with cyanotic heart disease. They may present with dyspnea, tachypnea and syncope. [4]
Long QT Syndrome(LQTS) The diagnosis of LQTS relies mainly on ECG findings and clinical history. When marked corrected QT (QTc) prolongation is present, the diagnosis is straightforward. When a prolonged QTc is identified after a syncopal event in the absence of acquired causes of QT prolongation the diagnosis of LQTS can be made. All first-degree family members has to be screened by ECG examinations. [5]
References
  1. WIGLE E. D., RAKOWSKI H., KIMBALL B. P., WILLIAMS W. G.. Hypertrophic Cardiomyopathy : Clinical Spectrum and Treatment. Circulation [online] 1995 October, 92(7):1680-1692 [viewed 04 August 2014] Available from: doi:10.1161/​01.CIR.92.7.1680
  2. BASSO CRISTINA, MARON BARRY J, CORRADO DOMENICO, THIENE GAETANO. Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. Journal of the American College of Cardiology [online] 2000 May, 35(6):1493-1501 [viewed 04 August 2014] Available from: doi:10.1016/S0735-1097(00)00566-0
  3. De Paepe, A., Devereux, R. B., Dietz, H. C., Hennekam, R. C., & Pyeritz, R. E. (1996). Revised diagnostic criteria for the Marfan syndrome. American journal of medical genetics, 62(4), 417-426. [viewed 04 August 2014] Available from: http://www.diagnosticcriteria.net/marfan/reprints/DePaepe-1996-AJMG-62-p417-426.pdf
  4. MITCHELL S. C., KORONES S. B., BERENDES H. W.. Congenital Heart Disease in 56,109 Births Incidence and Natural History. Circulation [online] 1971 March, 43(3):323-332 [viewed 04 August 2014] Available from: doi:10.1161/​01.CIR.43.3.323
  5. GOLDENBERG ILAN, MOSS ARTHUR J.. Long QT Syndrome. Journal of the American College of Cardiology [online] 2008 June, 51(24):2291-2300 [viewed 04 August 2014] Available from: doi:10.1016/j.jacc.2008.02.068

Investigations - for Diagnosis

Fact Explanation
Electrocardiogram (ECG) This study is indicated in all patients. Evidence of prolonged QT interval, short QT interval, epsilon wave (small positive deflection buried in the end of the QRS complex), Brugada sign, short PR, a W-P-W pattern, or other conditions should be sought.[1],[2]
2D Echocardiography Used to identify structural abnormalities in the heart. This may be considered to identify patients with potentially treatable causes of the arrest, especially pericardial tamponade and inadequate ventricular filling. [1],[2]
References
  1. KLEINMAN M. E., CHAMEIDES L., SCHEXNAYDER S. M., SAMSON R. A., HAZINSKI M. F., ATKINS D. L., BERG M. D., DE CAEN A. R., FINK E. L., FREID E. B., HICKEY R. W., MARINO B. S., NADKARNI V. M., PROCTOR L. T., QURESHI F. A., SARTORELLI K., TOPJIAN A., VAN DER JAGT E. W., ZARITSKY A. L.. Part 14: Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation [online] December, 122(18_suppl_3):S876-S908 [viewed 04 August 2014] Available from: doi:10.1161/​CIRCULATIONAHA.110.971101
  2. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144

Investigations - Fitness for Management

Fact Explanation
Blood gas analysis Done to evaluate hypoxemia, hypercapnia, and acidosis [1]
Pulse Oximetry Done as bed side investigation to monitor oxyhemoglobin saturation.[1]
References
  1. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144

Investigations - Followup

Fact Explanation
Electrocardiogram (ECG) Done to evaluate conduction impairment. An ambulatory electrocardiogram or an event monitor can be useful in capturing an ECG during an episode.
Serum electrolytes Done to assess serum sodium and potassium concentration as they are important in cardiac muscle conduction. [1]
References
  1. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144

Investigations - Screening/Staging

Fact Explanation
Electrocardiogram (ECG) Used in family screening programmes to identify arrhythmias. Also used in athletic screening. [1]
Genetic testing Cardiomyopathies, Arrhythmogenic Right Ventricular Dysplasia, Inherited arteriopathies such as Marfan syndrome can be detected by genetic testing. The genetic nature of many cardiac ion channelopathies predisposing youth to pediatric sudden cardiac arrest is being defined rapidly. But due to the high cost routine screening is not performed as of yet. [1]
References
  1. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144

Management - General Measures

Fact Explanation
Oxygen 100% oxygen is used in CPR for ventilation because there is inadequate information on the optimal concentration of oxygen. After the circulation is restored, systemic oxygen saturation is monitored. When the appropriate equipment is available titrate oxygen administration to maintain the oxyhemoglobin saturation ≥94%.[1]
Post resuscitation care The goal is to optimize cerebral perfusion and cardiac output by avoiding hyperthermia, maintaining normotension, normoglycemic and normocarbia and avoiding hypoxia. This is considered in patients who remain comatose after resuscitation. Patients have to be monitored in the post-Cardiac Arrest period ensures detection of clinical decline at the earliest time-point possible and minimizes secondary brain injury. In early hemodynamic optimization,the goal is to maintain a balance between delivery of oxygen systemically and overall oxygen demands. Monitoring via pulse-oximetry, arterial catheter, continuous electrocardiogram and temperature with general laboratory studies is important. Hypotension, dysrhythmias and low cardiac index have to be expected. In this situation initial intervention is the use of IV fluid to maintain right-heart filling pressures, with the use of inotropes and vasopressors. This hemodynamic stabilization will assure optimal cerebral perfusion. Seizures may occur during the post-Cardiac Arrest period. Prolonged seizures can worsen cerebral injury and hence prompt detection and treatment would be imperative to improving neurologic outcome. Therefore the use of continuous electroencephalographic (EEG) bedside monitoring should be considered as an important monitoring tool. Early hypothermia is shown to be beneficial in adults and neonates after Cardiac Arrest. In term neonates after hypoxic ischemic events, therapeutic hypothermia has shown to improve the neurologic outcome. Hypothermia should be considered for pediatric patients that remain comatose after cardiac Arrest. Conversely, hyperthermia (even an increase by 1°C) worsens neurological outcome and should be avoided.[2]
References
  1. KLEINMAN M. E., CHAMEIDES L., SCHEXNAYDER S. M., SAMSON R. A., HAZINSKI M. F., ATKINS D. L., BERG M. D., DE CAEN A. R., FINK E. L., FREID E. B., HICKEY R. W., MARINO B. S., NADKARNI V. M., PROCTOR L. T., QURESHI F. A., SARTORELLI K., TOPJIAN A., VAN DER JAGT E. W., ZARITSKY A. L.. Part 14: Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation [online] December, 122(18_suppl_3):S876-S908
  2. TRESS EE, KOCHANEK PM, SALADINO RA, MANOLE MD. Cardiac arrest in children J Emerg Trauma Shock [online] 2010, 3(3):267-272 [viewed 05 August 2014] Available from: doi:10.4103/0974-2700.66528

Management - Specific Treatments

Fact Explanation
Resuscitation - Basic life support In non-witnessed CA(cardiac arrest): the rescuer provides a brief period of CPR(cardiopulmonary resuscitation) before calling for professional help. In witnessed sudden collapse: the “Call first” approach should be followed, where the rescuer calls for professional help followed by initiation of CPR. Lone rescuer provides 30:2 compression–ventilation ratio for all age groups of patients. A Healthcare provider performing two-person CPR provides 15:2 compression–ventilation ratio for infants and children (of note, ratio of compression–ventilation is 3:1 for neonates). Infant CPR: the two thumb encircling hands technique is preferred for two-rescuer CPR. For lone rescuer CPR the two-finger technique is recommended . For child CPR, both one- and two-hand techniques can be used. When performing CPR, lower third of the sternum should be compressed, and the compression depth should be one-third of the anterior–posterior diameter of the chest.[1]
Cardioversion The pediatric dose for manual defibrillation for ventricular fibrillation is 2 J/kg. If this is not successful, the subsequent dose should be 4 J/kg. In children above 8 years or above 25 kg automatic defibrillation can be performed with a standard automatic external defibrillator (AED) . In children who are age between 1 and 8 years, using of a pediatric-attenuated AED is preferable if available. [1],[2],[3]
Airway Jaw-thrust maneuver or chin-lift/head tilt maneuver can be done to make the airway patent if trauma is not suspected. Permanent airway can be established via endotracheal intubation or ventilation with a bag and valve mask (BVM). Which method to use depends on the time needed for transport and the experience of the health care provider. Cuffed endotracheal tubes are acceptable in the pediatric population and are safe even for children <8 years old, excluding neonates. Other advanced airways such as the laryngeal mask airway have not been studied in children with CA . After an advanced airway is placed, chest compressions and ventilation occur without interruption. Compressions should occur at a rate of 100/min and ventilations should take place at a rate of 8–10/min.[1],[2],[3]
Medication during CPR The IV or IO routes should be used for administering medications during CPR in the pediatric population. During CA recommended dose of epinephrine is 0.01 mg/kg of the 1:10,000 concentration. Subsequent IV doses of epinephrine are recommended every 3–5 min during resuscitation at the same dose. Due to the potential for worse neurologic outcome high-dose epinephrine is no longer recommended. [1],[2],[3]
Adenosine Temporary atrioventricular (AV) nodal conduction block and interruption of reentry circuits that involve the AV node is done by adenosine. Its short half-life cause wide safety margin. Adenosine should be given only IV or IO, and it should be followed by a rapid saline flush to promote drug delivery to the central circulation. When adenosine is given IV, it should be administered as close to the heart as possible. [3]
Amiodarone Amiodarone causes slowing of AV conduction, prolonging of the AV refractory period and QT interval, and slowing of ventricular conduction (widens the QRS). Prior to administration expert consultation is strongly recommended. Monitoring of blood pressure and electrocardiogram (ECG) during intravenous administration of amiodarone has to be done. If the patient has a perfusing rhythm, administer the drug slowly (over 20 to 60 minutes); if the patient is in VF/pulseless VT, give the drug as a rapid bolus. Through its vasodilatory property amiodarone causes hypotension, and the severity is related to the infusion rate. With the aqueous form of amiodarone hypotension is less common. If there is prolongation of the QT interval or heart block the infusion rate has to be decreased. Infusion have to be stopped if the QRS widens to >50% of baseline or hypotension develops. Amiodarone also can cause bradycardia and torsades de pointes ventricular tachycardia. This drug should not be administered together with another drug that causes QT prolongation, as procainamide, without expert consultation. [3]
Atropine This is a parasympatholytic drug that accelerates sinus or atrial pacemakers and increases the speed of AV conduction. Due to its central effect small doses of atropine (<0.1 mg) may produce paradoxical bradycardia. In special circumstances such as organophosphate poisoning or exposure to nerve gas agents larger than recommended doses may be required. [3]
Calcium Calcium administration is not recommended for pediatric cardiopulmonary arrest except in hyperkalemia (excess potassium), hypermagnesemia (excess magnesium), hypocalcemia (low calcium), or calcium channel blocker overdose. If calcium administration is indicated either calcium chloride or calcium gluconate can be used. calcium chloride may be preferred in critically ill children, because it results in a greater increase in ionized calcium during the treatment of hypocalcemia. If the only venous access is peripheral, in the non arrest setting, calcium gluconate is recommended because it has a lower osmolality than calcium chloride and is therefore less irritating to the vein. [3]
Epinephrine The alpha-adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and then coronary perfusion pressure, which is a critical determinant of successful resuscitation from cardiac arrest. Vasoconstrictive α-effects of the epinephrine predominate in the doses used during cardiac arrest. Catecholamines and sodium bicarbonate should not administer simultaneously through an IV catheter or tubing because alkaline solutions such as the bicarbonate inactivate the catecholamines. [3]
Glucose As infants have a relatively high glucose requirement and low glycogen stores, infants may develop hypoglycemia when energy requirements rise. Therefore checking blood glucose concentration during the resuscitation and treat hypoglycemia promptly. [3]
Magnesium Is used for the treatment of torsades de pointes or for documented hypomagnesemia. Magnesium may cause hypotension if administered rapidly by causing vasodilation. [3]
Procainamide This prolongs the refractory period of the atria and ventricles and cause reduction in conduction velocity. Procainamide should be infuse very slowly (over 30 to 60 minutes) while monitoring the ECG and blood pressure. Infusion rate has to be decreased if there is prolongation of the QT interval, or heart block; the infusion has to be stopped if the QRS widens to >50% of baseline or hypotension develops. Should not administer together with another drug causing QT prolongation. Expert consultation is essential prior to using this drug for a hemodynamically stable patient.[3]
Sodium Bicarbonate Routine administration is not recommended . May be administered for treatment of some toxidromes or special resuscitation situations such as hyperkalemic cardiac arrest. [3]
Vasopressin There are insufficient evidence in making a recommendation n favour or against the routine use of vasopressin during cardiac arrest. Pediatric and adult case series/reports suggested that vasopressin or its long-acting analog (terlipressin), can be effective in refractory cardiac arrest when standard therapy fails. [3]
References
  1. TRESS EE, KOCHANEK PM, SALADINO RA, MANOLE MD. Cardiac arrest in children J Emerg Trauma Shock [online] 2010, 3(3):267-272 [viewed 05 August 2014] Available from: doi:10.4103/0974-2700.66528
  2. Pediatric Sudden Cardiac Arrest. PEDIATRICS [online] December, 129(4):e1094-e1102 [viewed 04 August 2014] Available from: doi:10.1542/peds.2012-0144
  3. KLEINMAN M. E., CHAMEIDES L., SCHEXNAYDER S. M., SAMSON R. A., HAZINSKI M. F., ATKINS D. L., BERG M. D., DE CAEN A. R., FINK E. L., FREID E. B., HICKEY R. W., MARINO B. S., NADKARNI V. M., PROCTOR L. T., QURESHI F. A., SARTORELLI K., TOPJIAN A., VAN DER JAGT E. W., ZARITSKY A. L.. Part 14: Pediatric Advanced Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation [online] December, 122(18_suppl_3):S876-S908 [viewed 05 August 2014] Available from: doi:10.1161/​CIRCULATIONAHA.110.971101