https://journal.chestnet.org/article/S0012-3692(16)38415-X/pdf

Definitions for Sepsis and Organ Failure and Guidelines for the Use of Innovative Therapies in Sepsis

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

Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.

https://science.sciencemag.org/content/sci/234/4775/470.full.pdf

Shock and tissue injury induced by recombinant human cachectin.

https://genoplivning.dk/wp-content/uploads/2013/07/european-resuscitation-council-guidelines-for-resuscitation-2010-section-4-adult-advanced-life-support.pdf

European Resuscitation Council Guidelines for Resuscitation 2010 Section 4 Adult advanced life support

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

A variant form of angina pectoris was observed in 23 patients. The clinical features, diagnosis, treatment, pathological physiology, and chemical changes are summarized. Chest pain developed when the patients were at rest or relatively inactive. Electrocardiograms, recorded during this type of anginal pain, showed an elevation of the S-T segment which disappeared when the pain stopped. The electrocardiogram may, therefore, show findings opposite to those of ordinary angina pectoris. In mild attacks the electrocardiogram may show spurious improvement. Sufficient diagnostic features are pointed out to allow for clinical diagnosis of typical cases, and two case histories illustrate the course and treatment of this condition.

Variantform of angina pectoris, previously undelineated syndrome.

The events preceding cardiac arrest were investigated in 132 critically ill patients on the basis of the hemodynamic, respiratory, and metabolic status prior to cardiac arrest. Approximately one-half of the patients had respiratory acidosis prior to cardiac arrest and only one of these patients ultimately survived. An additional one-fourth had metabolic acidosis due to progressive perfusion failure (shock), and none survived. In the remaining one-fourth, an immediate catastrophic and potentially preventable event accounted for cardiac arrest, and all but one of the long-term survivors were included in this group. In thirteen patients, obstruction or dislodgment of endotracheal tracheostomy tubes, or interruption of ventilation, was recognized as the immediate cause. In an additional 20 patients, cardiac arrest was associated with an adverse effect of a drug. Twelve instances of cardiac arrest were associated with central venous injection of aminophylline. The initial cardiac resuscitation attempt was effe...

Cardiac arrest in the critically ill. I. A study of predisposing causes in 132 patients.

https://www.amjmed.com/article/0002-9343(74)90593-2/pdf

Cardiac arrest in the critically III: II. Hyperosmolal states following cardiac arrest

Shock caused by gram-negative microorganisms. analysis of 169 cases.

A total of 410 critically ill patients in critical care units of six community hospitals were surveyed for a period of 31 days. A prognostic index of survival was derived by discriminant function analysis utilizing measurement of blood lactate, blood pressure, heart rate, arrhythmias, spontaneous respiration, urine volume, body temperature, age, and a five-point rating of clinical condition by the nursing staff. The case fatality rate in patients in whom blood lactate exceeded 2.7 mM was 50% fatality rate was 5% when lactate was less than 2.7 mM. The best prediction of survival was obtained by combining the plasma lactate and the five-point rating of the patient's condition. These data therefore could serve as a measure of the severity of illness at the time of admission and provide a quantitative guide for objective comparison of the effectiveness with which critical care services are delivered in acute care units. They can also provide an objective basis for priority assignment to cardiac care, intensive care, and other specialized units of the hospital

Herbert Shubin

Papers

Variantform of angina pectoris, previously undelineated syndrome.

Cardiac arrest in the critically ill. I. A study of predisposing causes in 132 patients.

Cardiac arrest in the critically III: II. Hyperosmolal states following cardiac arrest

Shock caused by gram-negative microorganisms. analysis of 169 cases.

Quantitation of severity of critical illness with special reference to blood lactate.