http://cardiologia.publicacionmedica.com/contenido/images/stemi_aha_2013.pdf

2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction

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

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

The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

/pdf/part-8-adult-advanced-cardiovascular-life-support-2010-344vtppnij.pdf

Part 8: Adult Advanced Cardiovascular Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

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

Objective: Experimental and clinical studies have implicated that α 1 and β-adrenergic effects of epinephrine significantly increased the severity of postresuscitation myocardial dysfunction by increasing myocardial oxygen consumption during ventricular fibrillation. This prompted experimental studies to investigate the effect of simultaneous blockade of α 1 - and β-actions of epinephrine during cardiopulmonary resuscitation. Design: Literature review. Results: Improved postresuscitation myocardial dysfunction was observed in epinephrine-treated animals after its α 1 - and β-actions were blocked, which were associated with less pos tresuscitation arrhythmia, lower blood lactate level, better neurologic recovery, and longer duration of survival. Conclusions: After simultaneous α 1 - and β-adrenergic blockade, epinephrine administered during cardiopulmonary resuscitation yielded improved postresuscitation myocardial functions and significantly better postresuscitation outcomes. (Crit Care Med 2006; 34[Suppl.]:S483-S485)

Simultaneous blockade of α1- and β-actions of epinephrine during cardiopulmonary resuscitation

The ultrasonographic evaluation of inferior vena cava (IVC) parameters, particularly the collapsibility index (CI), has been widely used in the assessment of the fluid responsiveness of critically ill patients, but the results are conflicting. In this study, we aimed to investigate the early change in CI after increased intravascular volume (IVV) induced by passive leg raising (PLR). A total of 145 healthy volunteers over 18 years old were enrolled between September and December in 2015. Before and 2 min after PLR, the maximum and minimum IVC diameters (maxIVC and minIVC) were measured by color Doppler ultrasonography, and the difference in CI (ΔCI) was calculated. The heart rate (HR) and noninvasive mean arterial pressure (MAP) were also monitored. We found that there was a significant increase in the mean maxIVC and minIVC values and a reduction in CI. Nevertheless, no significant differences in HR or MAP were observed before or 2 min after PLR. The baseline CI had no relationship with individual characteristics and a multiple linear regression analysis of the ΔCI and individual characteristics showed that age, baseline CI, and BMI were independent variables for ΔCI. In conclusion, IVC-CI measured by ultrasound is useful for the detection of early IVV change induced by 2 min PLR. However, its ability to detect the increased IVV value is influenced by age, BMI, and baseline CI. Moreover, only 50.3% of the subjects had an IVC-CI reduction of more than 10%, making IVC-CI of little value for clinical applications, due to its poor sensitivity.

Is the Collapsibility Index of the Inferior Vena Cava an Accurate Predictor for the Early Detection of Intravascular Volume Change

Acid-base balance during cardiopulmonary resuscitation.

Objectives: Although electrical shock is a unique and effective treatment for fatal arrhythmia, it produces myocardial dysfunction closely related to the intensity of shock delivered. The isolated contribution of defibrillator components to postshock contractile impairment is not yet securely established. We sought to evaluate contractile function in cardiomyocytes following electrical shocks with different peak currents, energies, and durations. We hypothesized that peak current may play a more important role than energy in determining postshock dysfunction. Prolongation of the duration may reduce contractile impairment. Design: Prospective, randomized, controlled study. Setting: University-affiliated research institute. Subjects: Male albino Sprague-Dawley rats. Interventions: We assigned 324 cardiomyocytes isolated from adult male rats to 11 groups having different waveforms (triangular and square), peak currents (derived from peak voltage gradients of 25 V/cm, 35.4 V/cm, 50 V/cm, 70.7 V/cm, and 100 V/cm), and durations (10 and 20 msecs) of shocks delivered. One single shock was given to each cardiomyocyte, and length shortening and Ca 2+ transients were recorded optically with fura-2 loading. Measurements and Main Results: Increase of peak current and corresponding energy caused more cells to have irregular beating (p < .001) and reduced length shortening (p < .001). This was associated with increased Ca 2+ abnormality (p < .05). Increasing peak current independent of energy significantly impaired postshock contractile function (p < .05), whereas the change of energy alone did not. Prolongation of duration independent of energy and peak current reduced postshock contractile impairment (p < .05). Conclusions: Peak current may play a more determinative role in producing postshock contractile dysfunction than does energy.

Wanchun Tang

Papers

Simultaneous blockade of α1- and β-actions of epinephrine during cardiopulmonary resuscitation

Is the Collapsibility Index of the Inferior Vena Cava an Accurate Predictor for the Early Detection of Intravascular Volume Change

Acid-base balance during cardiopulmonary resuscitation.

Individual effect of components of defibrillation waveform on the contractile function and intracellular calcium dynamics of cardiomyocytes.

Effects of ω-3 PUFA and ascorbic acid combination on post-resuscitation myocardial function.