There is increasing recognition that systematic post–cardiac arrest care after return of spontaneous circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is based in part on the publication of results of randomized controlled clinical trials as well as a description of the post–cardiac arrest syndrome. 1–3 Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury. 3,4 This section summarizes our evolving understanding of the hemodynamic, neurological, and metabolic abnormalities encountered in patients who are initially resuscitated from cardiac arrest. The initial objectives of post–cardiac arrest care are to ● Optimize cardiopulmonary function and vital organ perfusion. ● After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a comprehensive post–cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. ● Transport the in-hospital post–cardiac arrest patient to an appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care. ● Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

http://www.kardio.hu/feltoltott/dokumentumok/fajl_201148104747Cardiopulm_resuscit_Pt9_Post_cardiac.pdf

Part 9: Post-Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

It is important that the medical profession play a central role in critically evaluating the use of diagnostic procedures and therapies introduced and tested for detection, management, or prevention of disease. Rigorous, expert analysis of the available data documenting absolute and relative

/pdf/acc-aha-2008-guidelines-for-the-management-of-adults-with-4oqjti8ewr.pdf

ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: Executive summary - A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (writing committee to develop guidelines for the management of adults with congenital heart disease)

22q11.2 deletion syndrome (22q11.2DS) is the most common chromosomal microdeletion disorder, estimated to result mainly from de novo non-homologous meiotic recombination events occurring in approximately 1 in every 1,000 fetuses. The first description in the English language of the constellation of findings now known to be due to this chromosomal difference was made in the 1960s in children with DiGeorge syndrome, who presented with the clinical triad of immunodeficiency, hypoparathyroidism and congenital heart disease. The syndrome is now known to have a heterogeneous presentation that includes multiple additional congenital anomalies and later-onset conditions, such as palatal, gastrointestinal and renal abnormalities, autoimmune disease, variable cognitive delays, behavioural phenotypes and psychiatric illness - all far extending the original description of DiGeorge syndrome. Management requires a multidisciplinary approach involving paediatrics, general medicine, surgery, psychiatry, psychology, interventional therapies (physical, occupational, speech, language and behavioural) and genetic counselling. Although common, lack of recognition of the condition and/or lack of familiarity with genetic testing methods, together with the wide variability of clinical presentation, delays diagnosis. Early diagnosis, preferably prenatally or neonatally, could improve outcomes, thus stressing the importance of universal screening. Equally important, 22q11.2DS has become a model for understanding rare and frequent congenital anomalies, medical conditions, psychiatric and developmental disorders, and may provide a platform to better understand these disorders while affording opportunities for translational strategies across the lifespan for both patients with 22q11.2DS and those with these associated features in the general population.

/pdf/22q11-2-deletion-syndrome-3j52v782f8.pdf

22q11.2 deletion syndrome

In contrast to adults, cardiac arrest in infants and children does not usually result from a primary cardiac cause. More often it is the terminal result of progressive respiratory failure or shock, also called an asphyxial arrest. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis, progresses to bradycardia and hypotension, and culminates with cardiac arrest.1

Another mechanism of cardiac arrest, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), is the initial cardiac rhythm in approximately 5% to 15% of pediatric in-hospital and out-of-hospital cardiac arrests;2,–,9 it is reported in up to 27% of pediatric in-hospital arrests at some point during the resuscitation.6 The incidence of VF/pulseless VT cardiac arrest rises with age.2,4 Increasing evidence suggests that sudden unexpected death in young people can be associated with genetic abnormalities in myocyte ion channels resulting in abnormalities in ion flow (see “Sudden Unexplained Deaths,” below).

Since 2010 marks the 50th anniversary of the introduction of cardiopulmonary resuscitation (CPR),10 it seems appropriate to review the progressive improvement in outcome of pediatric resuscitation from cardiac arrest. Survival from in-hospital cardiac arrest in infants and children in the 1980s was around 9%.11,12 Approximately 20 years later, that figure had increased to 17%,13,14 and by 2006, to 27%.15,–,17 In contrast to those favorable results from in-hospital cardiac arrest, overall survival to discharge from out-of-hospital cardiac arrest in infants and children has not changed substantially in 20 years and remains at about 6% (3% for infants and 9% for children and adolescents).7,9

It is unclear why the improvement in outcome from in-hospital cardiac arrest has occurred, although earlier recognition and management of at-risk patients on general inpatient units …

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.110.971101

Part 14: Pediatric Advanced Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

https://www.hefssa.org/images/uploads/acc_aha_guidelines_for_adults_with_chd.pdf

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease

UNLABELLED Coagulopathies in children after cardiopulmonary bypass (CPB) are complex. There are very limited data correlating coagulation tests with postoperative bleeding. We evaluated coagulation changes after CPB and after the administration of coagulation products to 75 children. Baseline coagulation tests were obtained and repeated after protamine administration, after transfusion of individual coagulation products, and on arrival in the intensive care unit (ICU). Regression analysis demonstrated no baseline coagulation test to predict postoperative chest tube drainage. Weight and duration of CPB were determined to be the only predictors of bleeding. Further analyses demonstrated that children 8 kg. Postprotamine platelet count and fibrinogen level correlated independently with 24-h chest tube drainage in children 8 kg. Platelet administration alone was found to restore effective hemostasis in many patients. With ongoing bleeding, cryoprecipitate improved coagulation parameters and limited blood loss. Fresh-frozen plasma administration after platelets worsened coagulation parameters and was associated with greater chest tube drainage and more coagulation product transfusions in the ICU. Objective data to guide post-CPB component therapy transfusion in children are suggested. IMPLICATIONS Children <8 kg can be expected to have more severe coagulopathies, require more coagulation product transfusions, and bleed more after cardiopulmonary bypass. Correlations between coagulation tests and postoperative chest tube drainage are defined. Platelets and, if necessary, cryoprecipitate optimally restore hemostasis. Fresh-frozen plasma offers no benefits in correcting postcardiopulmonary bypass coagulopathies in children.

Predicting and Treating Coagulopathies After Cardiopulmonary Bypass in Children

https://www.annalsthoracicsurgery.org/article/S0003-4975(02)03568-3/pdf

One hundred pulmonary valve replacements in children after relief of right ventricular outflow tract obstruction.

In vitro flow experiments for determination of optimal geometry of total cavopulmonary connection for surgical repair of children with functional single ventricle

BackgroundMilrinone has been shown to increase cardiac output in children after cardiac surgery, but pharmacokinetic analysis has not been used to identify effective dose regimens. The purpose of this study was to characterize the pharmacokinetics of milrinone in infants and children and to apply th

The pharmacokinetics of milrinone in pediatric patients after cardiac surgery.

https://www.annalsthoracicsurgery.org/article/S0003-4975(03)00516-2/pdf

Vincent K.H Tam

Papers

Predicting and Treating Coagulopathies After Cardiopulmonary Bypass in Children

One hundred pulmonary valve replacements in children after relief of right ventricular outflow tract obstruction.

In vitro flow experiments for determination of optimal geometry of total cavopulmonary connection for surgical repair of children with functional single ventricle

The pharmacokinetics of milrinone in pediatric patients after cardiac surgery.

Deletion of chromosome 22q11.2 and outcome in patients with pulmonary atresia and ventricular septal defect.