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

Critical Care Medicine : Organizing and Staffing Intensive Care Units

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

An analyte monitor includes a sensor, a sensor control unit, and a display unit. The sensor has, for example, a substrate, a recessed channel formed in the substrate, and conductive material disposed in the recessed channel to form a working electrode. The sensor control unit typically has a housing adapted for placement on skin and is adapted to receive a portion of an electrochemical sensor. The sensor control unit also includes two or more conductive contacts disposed on the housing and configured for coupling to two or more contact pads on the sensor. A transmitter is disposed in the housing and coupled to the plurality of conductive contacts for transmitting data obtained using the sensor. The display unit has a receiver for receiving data transmitted by the transmitter of the sensor control unit and a display coupled to the receiver for displaying an indication of a level of an analyte. The analyte monitor may also be part of a drug delivery system to alter the level of the analyte based on the data obtained using the sensor.

Analyte Monitoring Device And Methods Of Use

We prospectively measured the end-tidal carbon dioxide concentration during 13 episodes of cardiac arrest in 10 critically ill patients receiving mechanical ventilation, to evaluate its usefulness as an indicator of circulatory status during cardiac arrest and resuscitation. The end-tidal carbon dioxide concentration decreased from a mean (+/- SD) of 1.4 +/- 0.9 to 0.4 +/- 0.4 percent after the onset of cardiac arrest. During precordial compression, it increased to 1.0 +/- 0.5 percent. The decreases in the end-tidal carbon dioxide concentration were associated with increases in systemic oxygen extraction (r = 0.79). Spontaneous circulation was restored on seven occasions. This was heralded by a rapid increase in the end-tidal carbon dioxide concentration, from 1.3 +/- 0.5 percent to an overshoot value of 3.7 +/- 2.1 percent, within approximately 30 seconds. The concentration then declined to a stable value of 2.4 +/- 1.8 percent four minutes after resuscitation. However, it remained 0.7 +/- 0.4 percent in six patients in whom resuscitative efforts failed to restore spontaneous circulation. These observations are consistent with experimental studies of cardiopulmonary resuscitation in pigs, in which the end-tidal carbon dioxide concentration varied directly with the cardiac output produced by precordial compression. We therefore propose that measurement of the end-tidal carbon dioxide concentration may be a practical, non-invasive method for monitoring blood flow generated by precordial compression during cardiopulmonary resuscitation and an almost immediate indicator of successful resuscitation.

End-Tidal Carbon Dioxide Concentration during Cardiopulmonary Resuscitation

Objective:Epinephrine has been the primary drug for cardiopulmonary resuscitation (CPR) for more than a century. The therapeutic rationale was to restore threshold levels of myocardial and cerebral blood flows by its alpha1 (α1) and alpha2 (α2)-adrenergic agonist vasopressor actions. On the basis of

Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation.

Objective To investigate the functional and metabolic changes in the myocardium after successful resuscitation from cardiac arrest. Design Prospective, randomized, sham-controlled study. Setting Animal laboratory at a university center. Subjects Domestic pigs. Interventions Electric induction of ventricular fibrillation by alternating current delivered to the right ventricular endocardium through a pacing electrode. Electric defibrillation was attempted after an interval of 12 mins of ventricular fibrillation, which included 4 mins of untreated ventricular fibrillation and 8 mins of precordial compression in 13 animals, seven of which were successfully resuscitated. Seven additional animals were randomized to serve as ``sham'' controls, in which cardiac arrest was not induced. Measurements and Main Results Left ventricular pressure-volume relationships utilizing the conductance method were obtained in conjunction with conventional hemodynamic and metabolic measurements at baseline and during a 6-hr interval after successful cardiac resuscitation. Progressive and striking increases in left ventricular volumes were observed after successful cardiac resuscitation. The end-diastolic volume increased from a prearrest level of 89 plus minus 21 mL to a maximum of 154 plus minus 53 mL (p less than .05) at 360 mins after successful resuscitation. The time-coincident end-systolic volume increased from 54 plus minus 21 to 126 plus minus 54 mL (p less than .05), such that the ejection fraction was reduced from 0.41 plus minus 0.10 to 0.20 plus minus 0.07 (p less than .05). Ventricular dilation was associated with marked reductions in stroke volume and ventricular work. However, compensatory increases in heart rate maintained cardiac output at levels that sustained adequate systemic oxygen delivery. The slope of the end-systolic pressure-volume relationships progressively decreased from 5.04 plus minus 1.88 to 2.00 plus minus 0.57 mm Hg/mL (p less than .05) at 360 mins after successful resuscitation. The volume intercept at left ventricular pressure of 100 mm Hg increased from 43 plus minus 19 to 94 plus minus 51 mL (p equals .03). Both the decrease in the slope and the increase in the volume intercept were characteristic of progressive impairment in contractile function. The rate of left ventricular pressure decrease was unchanged. Accordingly, no substantial changes in lusitropic properties were identified. Despite large increases in end-diastolic volume, the end-diastolic pressure remained unchanged. Conclusion Postresuscitation myocardial dysfunction in this animal model was characterized by impaired contractile function, decreased work capability, and ventricular dilation.

Myocardial dysfunction after successful resuscitation from cardiac arrest

Objectives: Both epinephrine and vasopressin increase aortic and carotid arterial pressure when administered during cardiopulmonary resuscitation. However, we recently demonstrated that epinephrine reduces cerebral cortical microcirculatory blood flow. Accordingly, we compared the effects of nonadrenergic vasopressin with those of epinephrine on cerebral cortical microvascular flow together with cortical tissue Po 2 and Pco 2 as indicators of cortical tissue ischemia. Design: Randomized, prospective animal study. Setting: University-affiliated research laboratory. Subjects: Domestic pigs. Measurements and Main Results: The tracheae of ten domestic male pigs, weighing 40 ± 2 kg, were noninvasively intubated, and the animals were mechanically ventilated. A frontoparietal bilateral craniotomy was created. Microcirculatory blood flow was quantitated with orthogonal polarization spectral imaging. Blood flow velocity in pial and cortical penetrating vessels measuring <20 μm was graded from 0 (no flow) to 3 (normal). Cerebral cortical tissue carbon dioxide and oxygen tensions (P b co 2 and P b o 2 ) were measured concurrently using miniature optical sensors. Ventricular fibrillation, induced with an alternating current delivered to the right ventricular endocardium, was untreated for 3 mins. Animals were then randomized to receive central venous injections of equipressor doses of epinephrine (30 μg/kg) or vasopressin (0.4 units/kg) at 1 min after the start of cardiopulmonary resuscitation. After 4 mins of cardiopulmonary resuscitation, defibrillation was attempted. Spontaneous circulation was restored in each animal. However, postresuscitation microvascular flows and P b o 2 were greater and P b co 2 less after vasopressin when compared with epinephrine. We observed that a significantly greater number of cortical microvessels were perfused after vasopressin. Conclusions: Cortical microcirculatory blood flow was markedly reduced after epinephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circulation in contrast to the more benign effects of vasopressin.

Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation.

To review the current management of in-hospital cardiac arrest and to identify variables that influence outcomes, OLDMEDLINE from 1950 to 1966 and MEDLINE from 1966 to March 2005 were searched using the keywords cardiopulmonary resuscitation, cardiac arrest, in hospital, and adult. Secondary sources were derived from review publications and personal communications by one of the authors. There is no secure evidence that the ultimate outcomes after cardiopulmonary resuscitation in settings of in-hospital cardiac arrest have improved in the >40 yrs that followed the landmark report by Kouwenhoven, Jude, and Knickerbocker, which launched the modern era of cardiopulmonary resuscitation. A paucity of objective measurements preclude secure protocols for sequencing of interventions and, even more, when to initiate and discontinue cardiopulmonary resuscitation. The preparedness of both physicians and nursing professionals to implement the published guidelines has itself been questioned. Whereas early access defibrillation with automated external defibrillators may be of benefit in out-of-hospital settings, there has as yet been no secure evidence that automated external defibrillators have had a favorable impact on in-hospital cardiopulmonary resuscitation when used on infrequent occasions by first responders. This contrasts with the much greater success of advanced life support providers and especially when electrical defibrillation is promptly performed by expertly trained personnel after onset of cardiac arrest. Outcomes are therefore improved in critical care settings and especially in coronary care units in which patients are continuously monitored.

Max Harry Weil

Papers

End-Tidal Carbon Dioxide Concentration during Cardiopulmonary Resuscitation

Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation.

Myocardial dysfunction after successful resuscitation from cardiac arrest

Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation.

In-hospital cardiac arrest.