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Que Hay De Nuevo En Reanimacion2009
- 1. QUE HAY DE NUEVO EN REANIMACIÓN Sergio Cárdenas Valdés Residente Anestesiología y Reanimación Universidad de Antioquia
- 7. Reanimación Cardiocerebral JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57
- 13. Ventilación pasiva JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57 Considerar intubación orotraqueal: después de completar 3 ciclos sin interrumpir las compresiones Permeabilizar vía aérea Dispositivo oro faríngeo Mascara de no reinhalación O2 altos flujos (10 lit/min)
- 14. Algoritmo paro cardiaco extrahospitalario < 5 minutos Análisis Análisis SEM Considere Intubación Insuflación pasiva de O2 JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57 < 2 seg < 2 seg < 2 seg Solo Compresiones torácicas 200 Compresiones torácicas 200 Compresiones torácicas 200 Compresiones torácicas < 5 minutos
- 15. Algoritmo paro cardiaco extrahospitalario > 5 minutos Análisis Análisis SEM Considere Intubación Insuflación pasiva de O2 JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57 < 2 seg < 2 seg < 2 seg Solo Compresiones torácicas 200 Compresiones torácicas 200 Compresiones torácicas 200 Compresiones torácicas 200 Compresiones torácicas
- 16. Masaje, análisis y descarga Análisis Masaje Carga y descarga Análisis, Carga , pausa y descarga Análisis, masaje y carga pausa y descarga
- 17. Masaje, análisis y descarga Cargar mientras se da masaje evitando pausas > 10 Seg
- 19. Supervivencia JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57 Mejoría de >300%
- 20. Current Opinion in Critical Care 2009, 15:189–197
- 21. Sobrevida – resultado neurológico JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57
- 22. Sobrevida JACC Vol. 53, No. 2, 2009. January 13, 2009:149–57
- 25. Cuidados post reanimación Considere antiarrítmico Aplique 2000 ml de SSN IV fría 4ºC en bolo Aplique hielo en ingle/axila/ cuello Vasopresor si hay hipotensión Control de la vía aérea Mantenga la ventilación 8 – 10 por minuto Unidad coronaria
- 32. Compresiones toracoabdominales Emergencias 2009;21:17-22
Notes de l'éditeur
- CPR: Survival Rates Disappointing Sudden cardiac death is a leading cause of mortality in the industrialized nations of the world and, accordingly, is a major public health problem In Sweden, the incidence of out-of-hospital ventricular fibrillation cardiac arrest has decreased from 33% in 1992 to 26% in 2005 (P<0.0001 for trend) [1 ]. At the same time, 1-month survival for patients with shock- able rhythms has increased from 12.7% in 1992 to 22.3% in 2005 (P<0.0001 for trend). Strategies to increase the success of defibrillation are evolving continuously.
- Cardiocerebral resuscitation (CCR) is a new approach for resuscitation of patients with cardiac arrest. It is composed of 3 components: 1) continuous chest compressions for bystander resuscitation; 2) a new emergency medical services (EMS) algorithm; and 3) aggressive post-resuscitation care. The first 2 components of CCR were first instituted in 2003 in Tucson, Arizona; in 2004 in the Rock and Walworth counties of Wisconsin; and in 2005 in the Phoenix, Arizona, metropolitan area. The CCR method has been shown to dramatically improve survival in the subset of patients most likely to survive: those with witnessed arrest and shockable rhythm on arrival of EMS. The CCR method advocates continuous chest compressions without mouth-to-mouth ventilations for witnessed cardiac arrest. It advocates either prompt or delayed defibrillation, based on the 3-phase time-sensitive model of ventricular fibrillation (VF) articulated by Weisfeldt and Becker. For bystanders with access to automated external defibrillators and EMS personnel who arrive during the electrical phase (i.e., the first 4 or 5 min of VF arrest), the delivery of prompt defibrillator shock is recommended. However, EMS personnel most often arrive after the electrical phase—in the circulatory phase of VF arrest. During the circulatory phase of VF arrest, the fibrillating myocardium has used up much of its energy stores, and chest compressions that perfuse the heart are mandatory prior to and immediately after a defibrillator shock. Endotracheal intubation is delayed, excessive ventilations are avoided, and early-administration epinephrine is advocated.
- cardiocerebral resuscitation (CCR) (Table 1) is a new approach to the resuscitation of patients with cardiac arrest that significantly improves neurologically intact survival Hallstrom et al. [21] demonstrated that complete instructions delivered in 62% of episodes for the victims receiving dispatcher-assisted conventional CPR and 81% of episodes for the victims receiving dispatcher-assisted chest compression-only CCR, and instructions for the chest compression-only CCR required 1.4min less to complete than instructions for the conventional CPR.
- Developed by the University of Arizona Sarver Heart Center Resuscitation Group, cardiocerebral resuscitation (CCR) (Table 1) is a new approach to the resuscitation of patients with cardiac arrest that significantly improves neurologically intact survival In each area, survival of patients with witnessed out-of-hospital cardiac arrest (OHCA) and shockable rhythm dramatically improved (3–5).
- The CCR method is composed of 3 important components: 1) continuous chest compressions (CCCs) for bystander resuscitation; 2) new emergency medical services (EMS) advanced cardiac life support (ACLS) algorithm; and 3) aggressive post-resuscitation care including therapeutic hypothermia and early catheterization/intervention (Table 1). CCR advocates CCC cardiopulmonary resuscitation (CPR) without mouth-to-mouth ventilations for witnessed cardiac arrest. For comatose patients postresuscitation, hypothermia and early cardiac catheterization (unless contraindicated), even in the absence of classic electrocardiograph (ECG) signs of infarction or ischemia, are recommended. Because these therapies are not available in all hospitals, the Arizona Bureau of Emergency Medical Services and Trauma is designating “Cardiac Arrest” hospitals, much as “Trauma One” hospitals are designated. This way, resuscitated but comatose patients post-resuscitation will have the best chance of neurologically normal recovery.
- Some blood flow continues for several minutes after cardiac arrest has occurred due to venous inflow into the heart promoted by adrenergic influences on vascular tone that maintains arterial pressure higher than venous pressure el ventriculo derecho se ingurgita con lo cual consume mas energia por eso se debe vaicar y hacer la descarga y luego volver a hacer masaje The concept of a dilated heart that must be decompressed – and kept decompressed as far as possible up to the moment of shock – is readily understood by rescuers who have this knowledge and provides powerful motiv- ation to the rescuer for according compression the pri- macy it merits in terms of priority in the routines and quality of delivery. Pauses in compressions ‘lose ground’ that takes time to be regained, and, so, must be mini- mized. Rescuers must also know that after successful delayed defibrillation, any contractions are initially very weak and the heart will dilate again unless aided by compressions started as soon as possible following the electrical discharge. They must be continued until there is clear evidence of a return of spontaneous circulation. Mean aortic pressure remains higher than mean venous pressure for about 5min; the difference here is labelled as (computed) coronary perfusion pressure. Note that the difference in the relaxation phase becomes negative for the first minute of compressions. Adapted with permission from Defibrillation The reason that shock success is reduced by brief interruptions in chest compressions is not entirely clear. It is known that coronary perfusion pressure declines rapidly when chest compressions are stopped, but it may be that the rapid dilation of the right ventricle and impairment of left ventricular myocyte stretch that occurs at this time makes restoration of a spontaneous circulation less likely
- 15 minutos fase metabolica corazon de piedra For ACLS, either prompt or delayed defibrillation is advocated, based on the 3-phase time-sensitive model of ventricular fibrillation (VF) articulated by Weisfeldt and Becker For bystanders with access to an automated external defibrillator (AED) and EMS personnel who arrive during the electrical phase (i.e., the first 4 or 5 min of VF arrest), prompt defibrillator shock is recommended However, EMS personnel most often arrive after the electrical phase—in the circulatory phase of VF Arrest During the circulatory phase of VF arrest, the fibrillating myocardium has used up much of its energy stores, and chest compressions that perfuse the heart are necessary and therefore advocated prior to and immediately after a defibrillator shock New Protocols for EMS Part of the rationale for the EMS portion of CCR is better understood in the context of the 3-phase time-sensitive model of cardiac arrest due to VF articulated by Weisfeldt and Becker (8). The first phase, the electrical phase, lasts about 4 to 5 min. During this phase, the most important intervention is defibrillation. This is why implanted cardioverter-defibrillators work and why the availability of AEDs and programs to encourage their use have saved lives in a wide variety of settings, including airplanes, airports, casinos, and some communities. The second phase to VF cardiac arrest is the circulatory phase, which lasts approxi- mately from minute 4 or 5 to minute 15. During this time, the generation of adequate cerebral and coronary perfusion pressures by chest compressions before and after defibrilla- tion is critical to neurologically normal survival. Ironically, if an AED is the first intervention applied during this phase, the subject is much less likely to survive (48). If pre-shock chest compressions are not provided, defibrillation during the circulatory phase almost always results in asystole or pulseless electrical activity (PEA). The general belief is that this may enhance the availability of intra- cellular metabolic substrate needed for effective contrac- tion. The value of prior compressions was first demonstrated by Cobb et al. [17] who used only 90 s of circulatory support before shocks were administered and improved survival thereby: with the low flows achieved this could hardly replete myocardial energy reserves. Moreover, evidence exists to show that high-energy phosphates are depleted relatively slowly. The high energy cost of fi brillation influences this only to a noncritical degree; experimentally, 50% of myocardial ATP is still present after 5min Other factors militate against any rapid effect on high-energy phosphate stores. In the arrested heart, the coronary perfusion pressure – measured as aortic minus right atrial pressure during the relaxation phase of compression that drives coronary flow – builds up only slowly as a compression sequence continues The intervals after an arrest that may be amenable to successful intervention have been described [27] as an electrical phase that corresponds to the period when the heart can respond to a shock, followed by a longer haemodynamic phase when compressions may still be effective. There follows the so-called metabolic phase which is associated with one final energy consuming intense contraction known to cardiac surgeons as stone heart; this is not at present responsive to treatment.
- Endotracheal intubation is delayed, excessive ventilations are avoided, and early Administration To avoid excessive ventilations of patients with cardiac arrest, which are common by both physicians and paramedics, the initial approach to ventilation is passive oxygen insufflation of epinephrine is advocated Another major problem during resuscitation efforts by EMS personnel is endotracheal intubation. Endotracheal intubation has adverse effects due to the relatively long interruptions of chest compressions during placement and adverse effects of positive-pressure ventilation and frequent hyperventilation (13,53).
- The ERC guidelines do not advocate its use in basic life support, partly because it could theoretically provoke ventricular fibrillation in someone who had a perfusing rhythm.
- “ Rescue breathing” as previously and currently advocated is a misnomer(termino erroneo) Most bystanders who witness a cardiac arrest are willing to alert EMS but are not willing to initiate bystander rescue efforts because they are not willing to perform mouth-tomouth ventilation. Training and certification in basic life support does not change this fact. Unfortunately, as late as January 2008, a scientific statement from the American Heart Association (AHA) that recognized the crucial need to increase bystander resuscitation had little new to offer but more vigorous layperson training (35). Bystanders have long been willing to do chest compression-only or CCC CPR for such individuals, an approach that has been shown to be dramatically better than doing nothing The second reason requiring mouth-to-mouth ventilations is not optimal is that even the best attempts by laypersons to do “rescue breathing” result in inordinately long interruptions of chest compressions during cardiac arrest (37), and long interruptions of chest compressions decrease neurologically normal survival For single laypeople recently certified in basic CPR, chest compressions are interrupted an average of 16 s to perform the recommended “2 quick breaths” (37). Recognizing the importance of delivering more chest compressions with less interruptions, the 2005 CPR guidelines were changed, recommending an increased compression to perfusion ratio (30:2), based not on experimental survival data but on consensus (15). Normal neurologic survival in our laboratory model of clinically realistic OHCA was better with CCC than with 30:2 compressions to ventilations when each set of chest compressions were interrupted for a realistic 16 s to deliver the 2 recommended assisted ventilations (39). During chest compressions for cardiac arrest, the forward blood flow is so marginal that any interruption of chest compressions decreases vital blood flow to the brain. A third reason that requiring mouth-to-mouth ventilations by bystanders is not optimal is that even if chest compressions are not interrupted, positive-pressure ventilation during cardiac arrest increases intrathoracic pressure, thereby decreasing venous return to the thorax and subsequent perfusion of the heart and the brain (40). This phenomenon is made worse when forceful ventilations are given while the chest is being compressed (14). Another concern with attempted rescue breathing during bystander CPR is the amount of air that enters the stomach rather than the lungs (41). Mouth-to-mouth ventilation can cause regurgitation in nearly 50% of patients, probably because of gastric insufflation (42). Lawes and Baskett (43) reported that 46% of nonsurvivors from cardiac arrest had full stomachs and 29% had evidence of pulmonary aspiration. In another study, 39% of patients receiving mouth-tomouth ventilations had signs of gastric regurgitation at the time of intubation (44). The evidence that immediate ventilations are necessary for sudden cardiac arrest victims is based neither on data during cardiac arrest nor on logic, because with the onset of VF-induced arrest, the pulmonary veins, left heart, and entire arterial system are filled with oxygenated blood. The important issue is to circulate such oxygenated blood to the tissues, particularly the brain and myocardium. The recommended ventilations do not increase arterial saturation—they only further delay the onset of critical chest compressions (45). Finally, mouth-to-mouth ventilations are not necessary in a significant number of victims of witnessed cardiac arrest because they initially gasp, and if chest compressions are started early and continued, many victims will continue to gasp and thereby provide physiologic ventilation (i.e., ventilations with decreasing intrathoracic pressures that facilitate venous return to the chest and heart). If chest compressions are initiated early, many subjects who are not gasping will begin to gasp. Because of these facts, it is important that bystanders be taught that “abnormal breathing” is either no or abnormal respirations and that abnormal respirations are apnea or gasping (46). Our experience is that laypersons may refer to this form of agonal breathing as “snoring.” Our recommendations that “rescue breathing” or assisted ventilations are not necessary during cardiac arrest should not be construed to mean that we do not think oxygen delivery is important. On the contrary, adequate tissue oxygenation delivery is critically important, and early in cardiac arrest, CCC provides this crucial oxygen delivery Cerebral Perfusion During Chest Compressions for Cardiac Arrest The importance of uninterrupted chest compressions in providing important cerebral perfusion was forcefully brought home to us as we listened to a recording of dispatch-directed CPR to a woman trying to resuscitate her husband. It must have taken some time for the paramedics to arrive because she returned later to the phone to ask the dispatcher, “Why is it that every time I press on his chest, he opens his eyes, and every time I stop to breathe for him, he goes back to sleep?” (47). What she was really asking was why is it every time I am doing chest compressions, he is not in coma, but every time I stop and perform so-called “rescue breathing,” he goes back into coma? During resuscitation efforts for cardiac arrest, brain perfusion is so marginal that any interruption in chest compressions, even for ventilations, has the potential of being deleterious. Definition The glossary on respiration and gas exchange, published in the Journal of Applied Physiology in 1973 [5], defines a gasp as a ventilatory movement consisting of an abrupt, sudden, transient inspiratory effort, which results in brief inspiration and expiration with a longer expiratory pause [6]. Gasping or agonal respirations typically pre- sent with a low respiratory rate, which may be irregular, and having a wide range of air volumes, from shallow efforts resulting in superficial air movements to rather deep breaths with impressive peak flow rates. Incidence and duration of active breathing or gasping During the untreated period of ventricular fibrillation cardiac arrest, the incidence has been reported to be as high as 100% of the investigated animals A single study, by Menegazzi and Check [18], docu- ments active breathing or gasping during an untreated ventricular fibrillation cardiac arrest period of more than 5min. Chest compressions initiate or prolong gasping In their ventricular fibrillation cardiac arrest model, Noc et al. [15] showed that gasping during chest com- pressions generated a minute ventilation of approxi- mately 3 l/min during the first minute of chest com- pressions (untreated downtime before initiation of resuscitation efforts was 4min) that subsequently declined to approximately 1 l/min after 7min of com- pressions. Consequently, higher levels of pO2 and lower levels of pCO2 are found in animals experiencing gasp- Ing Effect of gasping on cardiovascular functions Active respirations during cardiac arrest generate several potentially beneficial cardiovascular effects. During gasping inspiration, the decreasing intrathoracic pres- sure is associated with a decrease in intrathoracic and right atrial pressure, resulting in a pressure gradient promoting venous return to the heart [21]. These pres- sure gradients augment effective forward blood flow[17]. Improved cardiac output and cardiac contractility by gasping have been confirmed in a rat model [16]. Con- sequently, increased aortic pressure and coronary perfusion pressure [17,21], increased carotid blood flow [21], and decreased intracranial pressure with associated gasping during ventricular fibrillation [20] have been demonstrated. Despite this positive association between spontaneous breathing activity and improved outcome in cardiac arrest, it is not yet evident that this respiratory maneuver is really the cause for better survival. It may be an epiphenomenon reflecting sufficient perfusion to the brainstem. These results confirm that gasping is a frequent phenom- enon that is more prominent in the early stages of cardiac arrest, and therefore, has the potential to be especially confusing to lay rescuers, preventing the timely onset of resuscitation efforts. The proportion of surviving gaspers and surviving nongaspers in a study by Bobrow et al. [26 ] was identical to that reported 15 years ago by Clark et al. [7] in which 28 versus 27% of the overall survivors were gasping, whereas only 8 versus 9% of nonsurvivors were gasping, respectively. Set against this, animal experiments suggest that continuous chest compression without ventilation can deliver more oxygen to tissues than conventional cardiopulmonary resuscitation at least over a period of over 10min
- New Protocols for EMS Part of the rationale for the EMS portion of CCR is better understood in the context of the 3-phase time-sensitive model of cardiac arrest due to VF articulated by Weisfeldt and Becker (8). The first phase, the electrical phase, lasts about 4 to 5 min. During this phase, the most important intervention is defibrillation. This is why implanted cardioverter-defibrillators work and why the availability of AEDs and programs to encourage their use have saved lives in a wide variety of settings, including airplanes, airports, casinos, and some communities. The second phase to VF cardiac arrest is the circulatory phase, which lasts approxi- mately from minute 4 or 5 to minute 15. During this time, the generation of adequate cerebral and coronary perfusion pressures by chest compressions before and after defibrilla- tion is critical to neurologically normal survival. Ironically, if an AED is the first intervention applied during this phase, the subject is much less likely to survive (48). If pre-shock chest compressions are not provided, defibrillation during the circulatory phase almost always results in asystole or pulseless electrical activity (PEA). The previous recommendation for a stacked-shock protocol resulted in prolonged interruption of essential chest compressions for rhythm analysis before and after shocks during this circulatory phase of cardiac arrest (49,50). In-dwelling, high- fi delity, micromanometer-tipped, solid-state, pressure- measuring catheters typically show small pulsatile increases in aortic pressure post-shock (a phenomenon called “ pseudo-pulseless electrical activity”). Aortic pressures of 20/10 mm Hg are not uncommon in such a period. If hemodynamic support is provided by immediate chest compressions, these pressures often increase to 40/20 mm Hg and continue to increase until finally a perfusing and palpable pulse is realized. Without such immediate post- shock hemodynamic support provided by chest compres- sions, the aortic pressure will decline and soon be truly asystolic. Therefore, CCR calls for an additional 200 chest compressions immediately after the shock without a pause to assess the post-shock rhythm Recently, emphasis has been placed on minimizing the preshock pause, the time between stopping chest compressions and delivery of the Shock Stopping compressions for periods as short as just 10 s seems to reduce the chances of success- ful defibrillation During ventricular fibrillation, it is now well established that interruptions in chest compressions for periods as short as 10–20 s will reduce the chances of successful Defibrillation The reason that shock success is reduced by brief interruptions in chest compressions is not entirely clear. It is known that coronary perfusion pressure declines rapidly when chest compressions are stopped, but it may be that the rapid dilation of the right ventricle and impairment of left ventricular myocyte stretch that occurs at this time makes restoration of a spontaneous circulation less likely Use of single shocks will help to reduce the preshock pause, but further changes in defibrillation strategy will reduce this further; these changes include the use of resuscitation team debriefing using downloaded data from a CPR-sensing and feedback-enabled defibrillator, continuing chest compressions during charging and possibly during shock delivery and the use of com- pression artefact filtering to enable rhythm analysis with- out stopping chest compressions. The AHA guidelines [16] and Advanced Cardiovascular Life Support Provider Manual advocate resuming chest compressions if the defibrillator takes more than 10 s to charge. Using a manikin and qualified ALS instructors and providers, the effect on the preshock pause of using the AHA and ERC guidelines and manual paddles versus hands-free electro- des has been reported The study was under- takenusing a defibrillator with a fast charge time of 2 s. The longest preshock pause of 7.4 s (6.7–11.2) was associated with the ERC paddles technique; the AHA hands-free technique was associatedwith the shortest preshock pause of 1.5 s (0.8–1.5) Intra- venous adrenaline (1mg) is given as soon as possible, ideally within 10min of arrival of EMS personnel. Once this has happened, a shock can still decompress the heart by evoking a contraction but only for a very few minutes before a contraction becomes no more than an ineffective twitch, presumably influenced by progressive acidosis. At this stage, compressions are essential both because this is now the only means whereby the heart can be decompressed but also as the only means of improving the metabolic milieu that we hypothesize is likely to be influenced mostly by disturbances of potassium or pH The intervals after an arrest that may be amenable to successful intervention have been described [27] as an electrical phase that corresponds to the period when the heart can respond to a shock, followed by a longer haemodynamic phase when compressions may still be effective. There follows the so-called metabolic phase which is associated with one final energy consuming intense contraction known to cardiac surgeons as stone heart; this is not at present responsive to treatment.
- The study was under- takenusing a defibrillator with a fast charge time of 2 Hands free electrodes = Tiene pegados electrodos por lo que el analisis del ritmo no requiere tener pegadas las paletas
- Figure 2 Preshock pause time using American Heart Asso- ciation technique (stop cardiopulmonary resuscitation, analyse, cardiopulmonary resuscitation and charge, stop cardiopul- monary resuscitation, shock, restart cardiopulmonary resusci- tation) and European Resuscitation Council technique (stop cardiopulmonary resuscitation, analyse, charge, shock, restart cardiopulmonary resuscitation) with paddles and hands-free defibrillation systems Recently, emphasis has been placed on minimizing the preshock pause, the time between stopping chest compressions and delivery of the Shock Stopping compressions for periods as short as just 10 s seems to reduce the chances of success- ful defibrillation s.The longest preshock pause of 7.4 s (6.7–11.2) was associated with the ERC paddles technique; the AHA hands-free technique was associatedwith the shortest preshock pause of 1.5 s (0.8–1.5) (Fig. 2). If using a defibrillator with, for example, a charge time of 7 s, the estimated preshock pause using a hands-free system and the ERC guidelines is 12 s. The current ERC guidelines almost certainly over- emphasize the risks of defibrillation, and it is likely that continuing compressions during charging will become standard practice in the future. These data add evidence in support of the trendaway frommanual paddles to hands- free defibrillation.
- In-hospital cardiac arrest may be different. Hopefully, most in-hospital VF cardiac arrests can be detected and treated during the electrical phase with immediate defibril- lation. The National Registry of CPR of in-hospital cardiac arrests has shown that the majority are not VF but are rather non-VF arrests, many of which are noncardiac in etiology (51). In such cases, ventilation and chest compressions may be important.
- Ninguno recibio hipotermia terapeoutica, solo con minimizar las interrupciones en las compresiones toracicas. Bobrow et al. (4) instituted CCR (reported, as the editors required, as minimal-interruption cardiac resuscitation) in Arizona and found a >300% improvement (4.7% to 17.6%) in survival to hospital discharge in the subgroup of patients with witnessed cardiac arrest and shockable rhythm. These results are illustrated in Figure 3.
- The mean survival to hospital discharge with intact neurologic function was 15% in the 3 years prior and 48% during the year when CCR was provided (3). These 1-year results in a small number of witnessed arrests were almost too good to believe, suggesting a significant “ Hawthorne effect.” Neurologic intact survival rate at hospital discharge was 40% (including 1 patient who received hypothermia) (5). Thus, there may well have been a slight Hawthorne effect during the first year. Nevertheless, in the subset of patients with witnessed cardiac arrest and shock- able rhythm on arrival of the paramedics, there was dramatic improvement (15% to 40%) in neurologic intact survival at hospital discharge compared with the pre-CCR era
- The Third Pillar of CCR Post-Resuscitation Care Only about 25% of those initially resuscitated survive to leave the hospital. Among those initially resuscitated who do not survive long term, about one-third die from central nervous system damage, another one-third die from myo- cardial failure, and the final one-third from a variety of causes including infection and multiorgan failure
- La sobrevida al egreso hospitalario es solo de 25 % de los que fueron reanimados exitosamente: la mortalidad se debe a daño de snc, falla cardiaca y otras.. unde et al. (56) in Norway formalized their post- resuscitation care and pursued an aggressive approach with such patients. Their approach emphasized providing thera- peutic hypothermia to all who remained comatose post- resuscitation and performing early coronary angiography and percutaneous coronary intervention (PCI) in any pa- tients with possible myocardial ischemia as a contributing factor to their cardiac arrests. These investigators performed coronary angiography for any- one post-resuscitation with ST-segment elevation on their admission ECG regardless of the consciousness state. They also took the same approach to those without ECG ST- segment elevation, but in those for which there was nonethe- less a strong suspicion that myocardial ischemia was the underlying etiology of their cardiac arrests. A univariate anal- ysis of their data revealed that reperfusion therapy was by far the most influential factor on survival, with an odds ratio of >27 Finally, it is important to note that the neurologic status of long-term survivors during the experimental period of aggres- sive post-resuscitation care was excellent, with more than 90% having no neurologic deficits and 9% having mild deficits These data suggest strongly that significant improvement in survival to discharge and even 1-year survival can be achieved with an aggressive and standardized approach to post- resuscitation care. Reperfusion therapy, either PCI or coronary artery bypass graft, had the most profound effect on outcome with an adjusted multivariate analysis odds ratio of 4.5. Of note, many of these patients were transported directly from the emergency department to the PCI suite upon arrival to the hospital (i.e., in an aggressive manner paralleling the current recommendation for certain ST-segment elevation myocardial infarction [STEMI] patients) mportance of Therapeutic Hypothermia The use of mild (32°C to 34°C) therapeutic hypothermia for comatose post-resuscitated cardiac arrest victims is accepted Therapeutic hypothermia Two randomized controlled trials have demonstrated substantial improvement in survival and neurologic out- come when victims of witnessed prehospital ventricular fi brillation receive therapeutic hypothermia [20,21]. Sub- sequent meta-analyses, systematic reviews, and case con- trolled clinical series have given additional support to the positive improvement in outcome from this compara- tively simple and inexpensive procedure in patients with ROSC who remain comatose after cardiac arrest Despite these two randomized controlled trials along with the endorsement of the AHA and the International Liaison Committee on Resus- citation, therapeutic hypothermia is used in only a small minority of patients who are comatose after cardiac arrest Acute coronary intervention following resuscitation had shown improved survival compared with historical controls A recent editorial, summarizing the results of early catheterization and PCI after cardiac arrest, showed that from 13 clinical reports involving 744 patients, 62% sur- vived to discharge after resuscitation, with 82% of those survivors having good neurological function. Even more impressive, if both therapeutic hypothermia and early PCI were performed early in the postresuscitation period, survival rates of 78% were seen, with 81% of survivors having good neurological function. This combination seems to hold real promise for postresuscitation care.
- A todos los pacientes inconscientes post-reanimación Vs AHA post reanimacion por FV
- En el paro por OVACE se ve mejor rendimiento a las compresiones solas I consider that uninter- rupted chest compressions by compression-only CCR increase intrathoracic pressure, thereby create and sustain high airway pressures, and subsequently are useful to relieve complete foreign-body airway obstruction. How- ever, additional positive-pressure ventilations by conven- tional CPR force a foreign-body airway obstruction into the airway and may be harmful to relieve complete foreign-body airway obstruction.
- Compared with baseline data, the implementa- tion of ‘performance-integrated debriefing’ reduced the preshock pause, median (interquartile range), from 16.0 (8.5–24.1) to 7.5 (2.8–13.1) s (P<0.001). This implies that efficient team training, which stresses the importance of minimizing the delay between stopping chest compressions and shock delivery, can improve performance and reduce the preshock pause. Introduction Recent investigations have documented poor cardiopulmonary resuscitation (CPR) performance in clinical practice. We hypothesized that a debriefing intervention using CPR quality data from actual cardiac arrests (Resuscitation with Actual Performance Integrated Debriefing, or RAPID) would improve CPR performance and initial patient survival. Methods Rescuers at a university teaching hospital underwent weekly RAPID sessions between March, 2006 and February, 2007. During the intervention period, facilitators led debriefing discussions using actual performance data, obtained from a CPR-sensing defibrillator with audiovisual feedback capability, and highlighted deficiencies in CPR quality and defibrillation. These data were compared to an historical control in which a similar defibrillator was used. The main outcomes were objective metrics of CPR performance and initial return of spontaneous circulation (ROSC). Results CPR quality and outcome data from 123 patients resuscitated during the intervention period were compared to 101 patients in the baseline cohort. Compared to the control period, CPR quality parameters and defibrillation accuracy were improved (table). These were associated with a significant improvement in the unadjusted rate of ROSC (table). After adjusting for shockable vs. non-shockable rhythm, time and location of arrest, and patient demographics, the RAPID intervention was associated with a significant increase in the adjusted odds of ROSC (OR 1.84 [1.06 –3.20]; p=0.03). Conclusions The combination of RAPID and real-time audiovisual feedback improved CPR quality over the use of feedback alone, and was associated with an increased rate of ROSC . CPR sensing and recording devices allow for methods of debriefing that were previously available only for simulation based education; such methods have the potential to fundamentally alter resuscitation training and improve patient outcomes.
- Acronimo POD Animal and clinical studies* have shown that during CPR, the ResQPOD: • Doubles blood flow to the heart • Increases blood flow to the brain by 50% • Doubles systolic blood pressure • Increases survival rates • Increases the likelihood of successful defibrillation • Provides benefit in all arrest rhythms • Circulates drugs more effectively How do I know if the ResQPOD is working? How do I know if the ResQPOD is working? How do I know if the ResQPOD is working? How do I know if the ResQPOD is working? The ResQPOD works by increasing circulation. All ResQPODs are 100% tested prior to shipment to assure they are properly functioning. Measurements of blood flow and circulation must be made indirectly, especially in a patient undergoing CPR. The best and most rapid way to know the device is working is to measure end tidal carbon dioxide (ETCO2), an indirect measure of circulation. When ETCO2 is increased, it usually means that more blood is circulating; as blood passes through the lungs, more CO2 is removed proportionally to the increase in blood flow. Typically, ETCO2 increases by about 30% in a patient treated with the ResQPOD. This equates to a near doubling of blood flow to the heart. For the best comparison, you should measure ETCO2 prior to placement of the ResQPOD, and then about 3 minutes later. It sometimes takes up to 15 minutes to achieve maximum ETCO2 levels once the ResQPOD is in place. It is important to note that we do not advise taking time to measure ETCO2 prior to use of the ResQPOD as it only delays the benefit to the device. However, for those who want to see a difference, and thus know the ResQPOD is working, this is one way to measure it. D DD Does the ResQPOD provide positive end expiratory pressure (PEEP)? oes the ResQPOD provide positive end expiratory pressure (PEEP)? oes the ResQPOD provide positive end expiratory pressure (PEEP)? oes the ResQPOD provide positive end expiratory pressure (PEEP)? No. One animal study has shown that low levels of PEEP may improve the efficiency of CPR with the ResQPOD16 but there are no human studies evaluating both the ResQPOD and PEEP to date.
- The ResQPOD, an impedance threshold device (ITD), utilizes the interdependence of the body’s respiratory and circulatory systems to create a vacuum (negative pressure) within the chest during the recoil phase of CPR, which follows each chest compression. The ResQPOD regulates the influx of respiratory gases into the chest during the chest wall recoil (relaxation or decompression) phase, which lowers the intrathoracic pressure and draws more venous blood back to the heart. Improved blood return to the heart (preload) results in improved blood flow out of the heart (cardiac output) during the subsequent compression. Thus, despite its placement into the ventilation circuit, the ResQPOD is a circulatory enhancer device that works during chest compressions, specifically during the chest wall recoil phase of CPR. What effect will the ResQPOD have if used during the performance of continuous chest What effect will the ResQPOD have if used during the performance of continuous chest What effect will the ResQPOD have if used during the performance of continuous chest What effect will the ResQPOD have if used during the performance of continuous chest compressions without ventilations (e.g. com compressions without ventilations (e.g. com compressions without ventilations (e.g. com compressions without ventilations (e.g. compression pression pression pression- -- -only CPR)? only CPR)? only CPR)? only CPR)? ACSI is aware that some EMS agencies have elected to perform compression-only (or “hands-only”) CPR with ventilations withheld for a period of time. The American Heart Association recommends this CPR method only for lay rescuers who are not confident in their ability to perform ventilations. ACSI endorses the concepts of applying chest compressions rapidly and with minimal interruptions but does not support having trained rescuers or healthcare providers withhold ventilations due to the deleterious effects that low or no ventilations can have on hemodynamics during CPR. One recent study, which compared 10 breaths/minute vs. 2 breaths/minute in a porcine model of cardiac arrest found that “… during the first five minutes of CPR, 2 breaths/minute resulted in significantly lower carotid blood flow and brain-tissue oxygenation than did 10 breaths/minute. Subsequent addition of an impedance threshold device significantly enhanced carotid flow and brain-tissue oxygen tension, especially in the 10 breaths/minute group.”14 If an organization elects to provide compression-only CPR, they should not use the ResQPOD during the period of time when ventilations are withheld as atelectasis will occur over time, the patient will not receive supplemental oxygen, and will thus suffer from anoxia. When ventilations are resumed, the ResQPOD can be added. ACSI recommends that when the ResQPOD is used during CPR, positive pressure ventilations of at least 8 - 10/min should be provided. Does the ResQPOD interfer Does the ResQPOD interfer Does the ResQPOD interfer Does the ResQPOD interfere with the patient’s ability to exhale? e with the patient’s ability to exhale? e with the patient’s ability to exhale? e with the patient’s ability to exhale? No, the ResQPOD provides insignificant resistance to patient exhalation. Expired air leaves the patient through the ventilation port. No, the patient may be freely ventilated, at whatever compression to ventilation ratio and tidal volume the situation dictates.
- Objetivo: Intentar determinar en base a los artículos revisados si la compresión abdo- minal interpuesta (CAI) es una técnica a tener en cuenta en las maniobras de reanima- ción cardiopulmonar (RCP). Método: Se realizó una búsqueda bibliográfica vía internet por medio de PubMed® en- tre los meses de enero y diciembre de 2007 utilizando como palabra clave “compre- sión abdominal interpuesta” sola o asociada a “masaje torácico” o “reanimación car- diopulmonar”. Se seleccionaron sólo aquellos estudios en los que la CAI estaba implicada directamente en el estudio. Se encontraron un total 42 artículos, de los cua- les 17 eran revisiones bibliográficas o históricas y 25 eran ensayos clínicos de distintos tipos en los que a su vez se medían diferentes variables (presión arterial, gasto cardia- co, supervivencia,…). Posteriormente, se dividieron según el parámetro medido con el fin de comparar los resultados obtenidos en cada estudio. Resultados: Entre los estudios encontrados algunos muestran de las ventajas de la CAI y otros ponen en duda su utilidad, muy pocos con evidencia estadísticamente significa- tiva a favor de la CAI y siempre con respecto a parámetros muy concretos. Según los estudios revisados, la compresión abdominal interpuesta aumenta el retorno venoso mejorando el llenado de las cavidades cardiacas durantes la RCP y por tanto mejora el gasto cardiaco; causa un aumento de la presión diastólica de la aorta torácica lo que favorece la perfusión coronaria en la fase de relajación torácica; y por tanto aumenta la supervivencia de los pacientes que sufren una parada cardiorrespiratoria (PCR). Conclusiones: En ningún estudio de los revisados se encontró significación estadística en cuanto a la mayor eficacia de la CAI frente a la reanimación cardiopulmonar estándar (RCPst). Sin embargo, los parámetros medidos en muchos de ellos hacen pensar en que esta técnica podría ser realmente efectiva y por tanto podría justificar la realización de un estudio en el que se determinara si resulta realmente útil. Existe la duda de si la compresión abdominal provocará lesiones a este nivel durante la manio- bras de RCP. En alguno de los estudios revisados se realizaron autopsias a los pacientes fallecidos y en ninguno se encontraron lesiones abdominales atribuibles a la compresión abdominal. Por lo tan- to, en base a todo lo expuesto, creemos que la CAI puede ser efectiva. Por ello, parecería adecua- do que esta revisión fuese el punto de partida pa- ra la realización de un estudio que determine su efectividad o no en la RCP.
- Ewy [27 ] made a favorable comment on our SOS- KANTO study [15 ] and pointed out that mouth-to- mouth ventilation for nonrespiratory cardiac arrest was detrimental for eight reasons. First, requirement of the performance of mouth-to-mouth ventilation greatly decreases bystander-initiated BLS efforts, an important determinant of survival from out-of-hospital cardiac arrest. Second, survival is better in individuals with cardiac arrest who receive chest compression-only CCR than it is in those in whom no bystander rescue efforts were started until the actual or simulated arrival of EMS personnel. Third, mouth-to-mouth ventilations by bystanders require inordinately long interruptions of essential chest compressions. Fourth, during cardiac arrest, mouth-to-mouth or positive-pressure ventilation increases intrathoracic pressures, thereby reducing venous return to chest. Therefore, positive-pressure ventilation reduces the already marginal coronary and cerebral blood flow during cardiac arrest and resuscita- tion. Fifth, with sudden unexpected cardiac arrest, venti- lations are initially neither necessary nor logical, for with the onset of ventricular fibrillation-induced arrest, the pulmonary veins, the left heart, and the entire arterial system are filled with oxygenated blood, and the recom- mended ventilations do not increase arterial saturation. Sixth, mouth-to-mouth ventilation is not necessary in a significant number of victims of witnessed cardiac arrest because they initially gasp, and if chest compressions are started early and continued, many of these patients will continue to gasp and thereby provide physiological venti- lation (e.g., that with decreasing intrathoracic pressures that facilitates venous return to the chest). Seventh, survival from experimentally induced cardiac arrest is better with higher coronary perfusion pressures produced by forceful chest compressions. Eighth, in nonparalyzed animals in cardiac arrest, survival is dramatically better with chest compression-only CCR than with chest com- pressions and mouth-to-mouth ventilations, when chest compressions were interrupted for a realistic 16s to pro- vide the two mouth-to-mouth ventilations between each set of 15 chest compressions CCR by citizens or EMS personnel was equivalent or superior to conventional CPR for all adult patients with out-of-hospital cardiac arrest in terms of survival or neurological benefit.