ardiac arrest during anesthesia has become a rare event. The development of better monitoring, safer medications, adoption of clinical standards and advances in knowledge and training have all had a significant impact on patient safety. Despite this, cardiac arrest during anesthesia still occurs, and with prompt recognition, diagnosis and treatment can be successfully managed.

Although general anesthesia represents one aspect of health care where the risk of death is relatively low,¹ challenging surgical indications are now being extended frequently to higher-risk cardiovascular and elderly patients. Furthermore anesthetic procedures have extended outside the operating room (O.R.) into arenas such as the radiology and gastroenterology suites, and the role of the anesthesiologist has become prominent in the intensive care unit.
In summary the practice of anesthesiology and critical care medicine puts the anesthesiologist in a unique position to lead all in-hospital resuscitation in North America, with extension to prehospital care in many European emergency systems where they participate directly in ambulance rescue teams.

In this progressively challenging clinical environment, a major goal of the American Heart Association (AHA) has been to provide all health professionals with updated and evidence-based guidelines on resuscitation from cardiac arrest and management of dysrythmias to acute coronary syndrome and stroke. The 2005 AHA “Guidelines for CPR” represent the largest review of cardiac arrest and resuscitation literature ever published.^{2, 3} An extensive critical analysis of the literature (the last five years), which includes the level of evidence, is the result of a consensus conference organized by the International Liaison Committee on Resuscitation, or ILCOR,² and the “Cardiopulmonary Resuscitation Guidelines” have been published as a supplement in the journal Circulation.³ This comprehensive issue lists a class of recommendations that integrate the strength of the scientific evidence with application factors in the United States. Both publications are available free on the Web <www.circulationaha.org>.

One of the striking findings of the 2005 International Consensus Conference on Cardiopulmonary Resuscitation has been better awareness of the poor quality of chest compression provided at the scene of the arrest. Good CPR remains the foundation upon which adequate cerebral and coronary perfusion is built, while pharmacological intervention and defibrillation are used to enhance restoration of spontaneous circulation (ROSC).⁴

To achieve the goal of improving the quality of chest compressions delivered, simplification of CPR recommendations and strong messages were sought. AHA guidelines now emphasize that the rescuer should “push hard, push fast” (a compression rate of 100 per minute) on the chest while allowing full chest recoil and should minimize “dead time” periods of no compression. This is achieved in the focused professional rescue team by limiting time spent during pulse check (10 seconds), defibrillation and advanced airway insertion. Performing good chest compressions is fatiguing, as demonstrated by the reliable recording of acute deterioration of CPR quality within two minutes in mannequin models. This observation led to the recommendation that the rescuers should change “compressor” roles approximately every two minutes. Other simplifications of the algorithms included the elimination of differences in single-rescuer CPR technique for different ages and combining the pulseless electrical activity and asystole algorithms.

During the first minutes of CPR for ventricular fibrillation (VF), oxygen delivery is flow-dependent (cardiac output) and therefore more dependent on effective chest compressions than ventilation. During CPR, blood flow to the lungs is only about 30 percent of normal, so less ventilation than normal (fewer breaths and smaller volume) is needed to match ventilation with perfusion.

The above considerations led to the overall single most important change in the guidelines: the change of compression/ventilation ratio (C:V) to a universal 30:2 for single rescuers for victims of all ages (except newborns) and two-rescuer CPR for adult victims until an advanced airway device is inserted. The concern that a higher percentage of infants and children frequently develop cardiac arrest secondary to asphyxia has resulted in a more conservative approach on ventilation in this patient population, with a recommended C:V of 15:2 when two rescuers are available.

Anesthesiologists have traditionally learned to link patient’s cyclic blood pressure variation when positive pressure ventilation is applied with hypovolemia or lung over inflation (extremely good lung compliance or excessive positive pressure provided). A striking finding of the new guidelines, however, has been the recognition of frequent unintentional hyperventilation during CPR (too many breaths or large tidal volumes given) and its inherent risk for the patient’s survival.⁵ Excessive intrathoracic pressure can decrease venous return, thereby decreasing coronary and cerebral perfusion and effectiveness of CPR.

The recommended respiratory rate, inspiratory time and tidal volume also have been decreased from the earlier 2000 AHA guidelines and are limited to 8-10 per minute, one second and 500-600 mL, respectively. Because it is difficult to estimate tidal volume without a spirometer, each rescue breath provided should be sufficient to produce visible chest rise, a parameter that corresponds to about 500 to 600 mL in the average healthy adult under anesthesia.⁶

Two-rescuer CPR with an advanced airway is the most likely scenario of cardiac arrest we can encounter in the O.R. Once an advanced airway is in place for an infant, child or adult victim, the rescuers no longer need to deliver cycles of compressions interrupted with pauses for ventilation and ventilation paced every six to eight seconds. The danger of inadvertent hyperventilation in this scenario has been again emphasized.

Treatment of VF / Pulseless Ventricular Tachycardia (VT)
Evidence accumulated in the last few years suggests a very high first-shock success in eliminating VF and pulseless VT using biphasic waveforms. Therefore defibrillation attempts in this scenario have been limited at one every five C:V cycles (about two minutes) of CPR to allow the provider to assess ROSC by pulse check and electrocardiogram in the shortest possible time. Vasopressors are administered if VF or pulseless VT persists after the first or second shock. Epinephrine 1 mg remains the recommended dose, to be repeated every three to five minutes. A single dose of vasopressin (40 U) may be given to replace either the first or second dose of epinephrine. Importantly, lidocaine should be considered only if amiodarone is not promptly available, and after the first dose of vasopressors if VF or pulseless VT persists.

Treatment of Asystole/Pulseless Electrical Activity
For rhythms that do not respond to electrical shocks, vasopressors and fluid challenge continue to be the mainstay of therapy based on improvement in aortic blood pressure and coronary artery perfusion pressure until the cause of the event is rectified. Epinephrine (1 mg) is still recommended and may be administered every three to five minutes. One dose of vasopressin (40 U) may be substituted for either the first or second dose of epinephrine. In fact in one large out-of-hospital, prospective, randomized study, vasopressin (compared with epinephrine) improved ROSC for a subgroup of patients with asystole, suggesting that this drug may have a role in “late CPR patients” where this type of rhythm is more frequent.⁷ Atropine (1 mg) may still be considered for asystole or slow pulseless electrical activity, up to three doses. In general most drug doses are the same as those recommended in the 2000 AHA guidelines, with the exception of symptomatic bradycardia in which the recommended dose of atropine was halved to 0.5 mg to reduce the potential adverse effect of uncontrolled tachycardia after its administration.

Defibrillation
As stated above, the evidence accumulated in the last few years suggests a very high first-shock success of biphasic waveforms in eliminating VF or rapid VT.

The “Shock! Shock! Shock!” stacked sequence has been replaced by a single shock followed by immediate CPR at a five C:V cycle or two-minute intervals. The need for more “aggressive” chest compression has been emphasized to the level that it be considered before defibrillation if cardiac arrest is presumed to be ongoing for more than four to five minutes. Prehospital and in-hospital studies failed to identify one single “best dose” of defibrillation energy due to the complexity and diversity of defibrillator and protocols used. A guideline recommendation range now exists, however. The initial selected dose for attempted defibrillation is 150 J to 200 J for a biphasic truncated exponential waveform and 120 J for a rectilinear biphasic waveform. If the biphasic waveform is unknown, 200 J is recommended. The follow-up shock approach is unchanged, with the second dose being at least the same or higher energy. Monophasic defibrillators are disappearing from the production chain. Because they are less efficient, the recommended dose has been set immediate to the highest dose of 360 J.

Conclusions
The newer 2005 AHA guidelines represent the current state-of-the-art, evidence-based medicine applied to resuscitation post cardiac arrest. The epidemiology of cardiac arrest in the O.R., however, is unique, and special circumstances still apply when acute coronary syndrome or a hypoxia/hypercarbia scenario is observed when a regional or general anesthetic is provided. In fact there are intuitive differences in patient management when the health care provider has prior knowledge of a patient’s medical history, is immediately aware of the probable cause of arrest and begins medical management within seconds.

In this continuously changing environment, it is time to provide our specialty with solid clinical guidelines when “an O.R. code” occurs — a challenging but perfect task for the ASA Committee on Critical Care Medicine.

References:
1. Lagasse RS. Anesthesia safety: Model or myth? A review of the published literature and analysis of current original data. Anesthesiology. 2002; 97:1609-1617.
2. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Circulation, 112(22 suppl, November 29), 2005.
3. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Circulation, 112(24 suppl, December 13), 2005.
4. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA. 2005; 305-310.
5. Aufderheide TP, Lurie KG. Death by hyperventilation: A common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med. 2004; 32(9):S345-S351.
6. Baskett P, Nolan J, Parr M. Tidal volumes which are perceived to be adequate for resuscitation. Resuscitation. 1996; 31(3):231-234.
7. Wenzel V, Krismer AC, Arntz R, Sitter H, Stadlbauer KH, Linder KH, for the European Resuscitation Council Vasopressor During Cardiopulmonary Resuscitation Study Group: A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004; 350:105-113.

Andrea Gabrielli, M.D., F.C.C.M., is Associate Professor of Anesthesiology and Surgery, Department of Anesthesiology, University of Florida, Gainesville, Florida. He is ASA liaison to the American Heart Association.

Steven A. Robicsek, M.D., Ph.D., is Assistant Professor of Anesthesiology, University of Florida, Gainesville, Florida.