CPR – 50 Years On: Part 2

Although successful return of spontaneous circulation (ROSC) and survival to hospital discharge (STD) depend upon the provision of high-quality CPR, data exist to show that resuscitation quality is often lacking. Researchers from the University of Chicago reported inadequate compression rates by medical house staff in 28% of events, insufficient compression depth (37%), excessive ventilation (61%), and zero compressions for the first 5 min of resuscitations (40%) (Abella et al. JAMA. 2005;293[3]:305).

An analysis of outside the hospital cardiac arrest (OHCA) resuscitations in experienced Norwegian emergency medical technician (EMT) personnel showed similar inadequacies in compression depth and excessive hands-off time (Wik et al. JAMA. 2005;293[3]:299). Compared with continuous compressions, hands-off no flow time is especially deleterious in animal models of CPR, as coronary and carotid blood flow falls rapidly and rises to much lower levels when compressions are resumed (Steen et al. Resuscitation. 2003;58[3]:249). Failure of adequate compressions causes delayed peak blood levels of epinephrine and blunted coronary perfusion pressure (Edelson et al. Resuscitation. 2006;71[2]:137). Poor compressions with long preshock pauses are less likely to produce successful defibrillation than are adequate compressions with shorter pauses (Pytte et al. Resuscitation. 2006; 71[3]:369). Incomplete release after a compression (also known as “leaning”) results in elevated intrathoracic pressure, which will also cause decreased coronary perfusion and decreased resuscitation success. Excessive leaning was demonstrated in 46% of a consecutive series of OHCA resuscitations in Wisconsin (Aufderheide et al. Resuscitation. 2005; 64[3]:353). Adequate quality of compressions is a major focus of the newly released 2010 AHA CPR guidelines (Field et al. Circulation. 2010;122[183]:S640 or www.Heart.org/CPR).

Though prompt defibrillation is essential in the treatment of shockable rhythms, an analysis of a national registry of inpatient arrests (NRCPR) revealed that defibrillation was delayed more than 2 min in 30% of 6,789 cases reviewed. A dose-dependent reduction in the likelihood of successful ROSC and STD follows increasing delay in defibrillation (Chan et al. N Engl J Med. 2008; 358[1]:9).

The 2005 AHA CPR guidelines called for the development of methods to improve the quality of CPR and the implementation of quality improvement processes, including monitoring of CPR quality. A 2007 international expert consensus panel recommended that compression depth, percent of incomplete release, compression rate, compression: relaxation ratio, hands-off no flow time, and the proportions of time with ventilation rate over 15 breaths per minute or zero ventilation be recorded, reported, and tracked (Kramer-Johansen et al. Resuscitation. 2007;74[3]:406). The use of newer defibrillators with recording and reporting capability makes collection of these data more feasible.

Cardiocerebral Resuscitation
In consideration of several physiologic principles discussed above, a group in Arizona, led by Gordon Ewy, proposed replacing rescue breathing with continuous oxygen insufflation and continuous compressions. With the addition of postresuscitation hypothermia and aggressive coronary revascularization of survivors, the Arizona system, Cardio Cerebral Resuscitation (CCR) (Ewy and Kern. J Am Coll Cardiol. 2009;53[2]:149), produced substantial improvements in survival in several OHCA studies (Kellum et al. Am J Med. 2006;119[4]:335).

The early success of the CCR approach prompted the AHA to endorse the 2010 CPR guidelines compressiononly resuscitation for OHCA for rescuers without “confident” ACLS skills while continuing to advocate 30:2 rescue breathing by trained rescuers. CCR has been validated only for OHCA ventricular tachycardia/fibrillation (VT/VF) events and has not been studied for nonshockable OHCA rhythms or IHCA events. CCR is not intended for primary respiratory or asphyxic arrests where substantial depletion of body oxygen stores occurs. Continuous compression may potentially increase rescuer fatigue, with deterioration in the quality of compressions.

Mechanical Devices
Cardiac filling occurs during the decompression phase of a CPR cycle. Passive reexpansion of the chest wall generates negative pleural pressure and enhances venous return. This advantage is lost during positive pressure rescue breathing. Addition of an impedance valve into a bag-mask ventilation circuit can block inspiratory airflow during decompression and allow passive chest wall relaxation to generate negative pleural pressure and enhance cardiac filling (Pirracchio et al. Curr Opin Crit Care. 2007;13[3]:280). Reviewers for the International Liaison Committee on Resuscitation (ILCOR) described the impedance threshold device (ITD) as “fairly effective,” and the AHA gave its adjunctive use a Class IIb recommendation for trained personnel in the newly released CPR guidelines.

Another recent study carried out with mannequins and an audiovisual feedback– capable defibrillator demonstrated rescuer fatigue, manifested by a decrease in compression depth without loss of compression rate, after 90 sec or longer of metronome-guided compressions. It is not clear whether hands-off time associated with a more frequent change of rescuers would offset any advantage gained in compression quality (Sugerman et al. Resuscitation. 2009; 80[9]:981). To address problems with rescuer fatigue and inadequate rate and depth of compressions, automated battery-powered compression and compression-decompression devices have been tested. These devices have been associated with improved secondary outcomes (endtidal CO₂, myocardial blood flow, blood pressure, and coronary and carotid perfusion pressures), but neither device introduced in the last 5 years has produced better survival outcomes, possibly due to the hands-off time required for initial deployment (Perkins et al. Curr Opin Crit Care. 2010;16[3]:203). Their routine use was not endorsed in the 2010 AHA guidelines, but they may be considered (Class IIb) by qualified personnel when there are difficulties with manual compression.

The presence of a hard surface (eg, a backboard) has improved the effectiveness of compressions; conversely, the lack of a hard surface has caused recording defibrillators to overestimate the depth of chest compression. Optimal compression depth has been linked to the bed being at the height of the rescuer’s knee (Cho et al. Emerg Med J. 2009;26[11]:807).

Improving CPR Education
Deficiencies in rescuer performance may indicate a need for improvement in the education and maintenance of resuscitation skills. Knowledge gained from traditional advanced cardiopulmonary life support/basic life support (ACLS/BLS) training deteriorates rapidly. ACLS graduates have been found to perform only 31% of appropriate interventions in real arrest events; skills retention in ACLS-trained nurses may be as low as 30% only 3 months after training.

Frequent refreshers have been demonstrated to improve resuscitation skills retention. Simulation-based ACLS training has resulted in better initial performance than has instructor-only training. Realtime audiovisual feedback from smart defibrillators may improve training effectiveness but may be ignored during the stress of a real arrest event (Seethala et al. Curr Opin Crit Care. 2010; 16[3]:196). The use of a weekly, structured debriefing of house staff with a morbidity/mortality format resulted in improvement in CPR quality and a 33% improvement in ROSC but no improvement in STD (Edelson et al. Arch Intern Med. 2008;168[10]:1063). An abstract from a group in San Diego reported improved survival outcomes with a resuscitation bundle (simulation-based training, a rapid response team, adherence to the principles of CCR, and feedback defibrillators) (Sell et al. Circulation. 2009;120:S1441). In the new 2010 guidelines, the AHA gave Class I recommendations to competency-based assessment in CPR courses, skills retesting within the 2-year certification cycle, the use of videos for consistent training, and emphasis on teamwork and leadership skills, as well as debriefing.

Postarrest Care
The post–cardiac arrest state is associated with 60% to 65% mortality for both OHCA and in-hospital events. Nolan and colleagues (Nolan et al. Resuscitation. 2008;79[3]:350) described these clinical problems as the post–cardiac arrest syndrome (PCAS), consisting of anoxic and ischemic brain injury, cardiac dysfunction, and systemic ischemia-reperfusion injury complicated by persistence of the underlying cause of the arrest.

Brain injury is associated with “neuroexcitotoxicity,” calcium dysregulation, free radical production, protease cascades, cell death and apoptosis, impaired microperfusion and macroperfusion, and dysautoregulation. Cardiac dysfunction (tachycardia, hypotension, elevated left-sided filling pressures, and decreased cardiac output) is seen in 50% of patients with PCAS. Hypotension, in particular, carries a twofold risk of death.

The cytokine profile associated with ischemia-reperfusion injury in PCAS is similar to that seen in sepsis and has led to suggestions that PCAS may be managed according to similar principles. Mild hypothermia after cardiac arrest (HACA) has been shown to improve survival and neurologic outcomes in select patients with OHCA VT/VF arrests, though the original 2002 reports restricted HACA to only 8% of events (Hypothermia After Cardiac Arrest Study Group. N Engl J Med. 2002;346[8]:549).

In the 2010 CPR guidelines, the AHA continues to recommend (Class I) that induced hypothermia be employed for all patients still comatose after ROSC for VT/VF OHCA and considered (Class IIb) for all comatose arrest patients resuscitated from any IHCA and from nonshockable OHCA events.

There is a paucity of clinical data to absolutely support extension of HACA to these other groups, and the potential complications of hypothermia (shivering, bradycardia, electrolyte abnormalities, hyperglycemia, increased infection, and decreased drug clearance) need to be considered (Arrich et al. Cochrane Database Syst Revs. 2009; 4:CD004128).

Some groups have integrated HACA and the principles of early goal-directed therapy for sepsis to set protocols for care of patients with PCAS. In addition to HACA, cardiac dysfunction is managed by maintaining a central venous pressure at 8 to 12 mm Hg, a mean arterial pressure of 65 to 100 mm Hg, using dobutamine drip and intra-aortic balloon pump, if necessary. Urine output and lactate levels are reported as being more useful than central venous oxygen saturation.

Hemoglobin value is maintained at 9 to 10 mg/dL. Patients are ventilated to normocapnia. Hyperoxia is avoided; oxygen saturation is kept at 94% to 96%.

Hypoglycemia is considered far more dangerous than hyperglycemia; blood sugars are maintained between 100 and 180 mg/dL.

Electrolytes are normalized as much as possible. No randomized trials are currently available to confirm the utility of PCAS protocols, but two small trials with historical controls demonstrated a doubling of survival for OHCA patients, irrespective of initial rhythm (Sunde et al. Resuscitation. 2007;73[1]:29; Gaieski et al. Resuscitation. 2009; 80[4]:418).

An organized multisystem approach to the management of PCAS is endorsed and discussed in detail in one of the more important new sections of the 2010 AHA CPR guidelines.

Conclusion
Cardiac arrest remains a common and generally deadly problem, 50 years after Kouwenhoven. We have made progress in our ability to restart stopped hearts, but we can do better.

Improved training, frequent refresher training, feedback, and debriefing should lead to better resuscitation performance and, hopefully, to better outcomes.

Systematic analysis of the quality of our CPR performance should help distinguish the elements of the ACLS and BLS protocols that are truly important. Advances in the systematization of care provided to the post–cardiac arrest patient have the potential to yield greater improvements in our desired end point, which is neurologically intact survival to discharge.

Some of these elements have now been introduced in the 2010 revision of the international CPR guidelines, but the results of systematic quality monitoring and care guided by protocols are not likely to be seen before the 2015 guideline cycle.

Dr Eric G. Honig, FCCP
Pulmonary, Allergy, and Critical Care Medicine
Emory University School of Medicine
Atlanta, GA

Editor's Insight
This article concludes Dr Honig’s apt review of recent advances in CPR, but it does not suffice as a comparison of the 2005 and 2010 guidelines. Please access the 2010 American Heart Association Guidelines for CPR and ECC to review current key recommendations, such as the new sequence for institution of basic life support, a recommended compression depth of 2 inches, a compression rate of at least 100 beats per minute, and compressiononly CPR for untrained rescuers, among others (Field, et al. Part 1: Executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122[183]:S640 or www.Heart.org/CPR).