Services on Demand
- Cited by SciELO
- Access statistics
- Similars in SciELO
Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.61 no.5 Campinas Sept./Oct. 2011
Luiz Fernando dos Reis FalcãoI; David FerezII; José Luiz Gomes do AmaralIII
IPost-graduate student of the Anesthesiology, Pain and Intensive Care Medicine Discipline of the UNIFESP-EPM
IIProfessor of the Anesthesiology, Pain and Intensive Care Medicine of the UNIFESP-EPM
IIISenior Professor of the Anesthesiology, Pain and Intensive Care Medicine of the UNIFESP-EPM
BACKGROUND AND OBJECTIVES: The new cardiopulmonary resuscitation (CPR) guidelines emphasize the importance of high-quality chest compressions and modify some routines. The objective of this report was to review the main changes in resuscitation practiced by anesthesiologists.
CONTENTS: The emphasis on high-quality chest compressions with adequate rate and depth allowing full recoil of the chest and with minimal interruptions is highlighted in this update. One should not take more than ten seconds checking the pulse before starting CPR. The universal relationship of 30:2 is maintained, modifying its order, initiating with chest compressions, followed by airways and breathing (C-A-B instead of A-B-C). The procedure "look, listen, and feel whether the patient is breathing" was removed from the algorithm, and the use of cricoid pressure during ventilations is not recommended any more. The rate of chest compressions was changed for at least one hundred per minute instead of approximately one hundred per minute, and its depth in adults was changed to 5 cm instead of the prior recommendation of 4 to 5 cm. The single shock is maintained, and it should be of 120 to 200 J when it is biphasic; and 360 J when it is monophasic. In advanced cardiac life support, the use of capnography and capnometry to confirm intubation and monitoring the quality of CPR is a formal recommendation. Atropine is no longer recommended for routine use in the treatment of pulseless electrical activity or asystole.
CONCLUSIONS: Updating the phases of the new CPR guidelines is important, and continuous learning is recommended. This will improve the quality of resuscitation and survival of patients in cardiac arrest.
Keywords: Cardiopulmonary Resuscitation; Heart Arrest; Heart Massage.
The knowledge of cardiopulmonary resuscitation (CPR) maneuvers is a priority for all health care professionals 1. Anesthesiologists constantly deal with critical situations and are prone to witness episodes of cardiac arrest depending on patient's status, surgery, and changes resulting from the anesthetic process. In this environment, current knowledge and quick and precise attitudes determine the prognosis and survival free of sequelae.
The incidence of cardiac arrest during anesthesia varies in the literature ranging from 1:82,641 to 1:2,500 2,3. The main causes are related to changes in physical status (23.9:10,000) followed by surgical complications (4.64:10,000), and isolated anesthetic complications (1.71:10,000) 4.
In 1960 a group of cardiopulmonary resuscitation pioneers combined mouth-to-mouth resuscitation with chest compressions to create cardiopulmonary resuscitation, the saving method we currently call "CPR". This action when performed immediately after a sudden cardiac arrest can duplicate - and even triplicate - the survival chances of a victim. With its evolution, in 1992 the International Liaison Committee on Resuscitation (ILCOR), which meets twice a year to provide a discussion and coordination forum of all aspects of cardiopulmonary resuscitation, was created 5. On October 18, 2010, it resulted in the last publication with the new recommendations for the care of patients with cardiorespiratory arrest (CRA) and urgent cardiovascular care. The objective of this report was to present in a simplified and objective way the new recommendations for CPR procedures according to the ILCOR guidelines.
BASIC LIFE SUPPORT
Basic Life Support (BLS) is the pillar of care for patients in cardiorespiratory arrest aiming at maintaining oxygenation and perfusion of vital organs through continuous maneuvers 6. The fundamental aspects of BLS include the immediate recognition of cardiac arrest and activation of the emergency response team, early CPR, and fast defibrillation.
According to this new guideline a great emphasis has been given to the quality of care with rapid and strong chest compressions, and defibrillation and advanced care should be given in a way to minimize interruptions in CPR 7. The first rescuer should rapidly evaluate the presence of cardiac arrest by calling the patient and identifying apnea or respiratory distress, such as gasping 8. Even with the delay and difficulty of verifying the pulse 9, the recommendation is still the same for the health care professional, and it should not take more than ten seconds 10.
Chest compressions consist of rhythmic and strong compressions in the lower half of the sternum, and they should be quickly performed in all cardiac arrest patients 11-13. They are effective when applied intensely and quickly, with a rate of at least one hundred per minute and at a depth of at least 5 cm. Full chest recoil should be observed after each compression allowing the heart to be completely filled with blood before the next compression. The compression-ventilation ratio of 30:2 has been maintained until the insertion of an advanced airway device, at which point they will become continuous chest compressions (at least one hundred per minute) and one ventilation every six to eight seconds (eight to ten ventilations per minute). Figure 1 shows the complete algorithm of basic life support for a health care professional.
Fatigue of the person performing chest compressions can lead to inadequate rate and depth of chest compressions 14-16. Significant fatigue with superficial compressions is common after one minute of CPR. When two or more rescuers are available, taking turns every two minutes (or five cycles of compression-ventilation at a 30:2 ratio) is reasonable to prevent a reduction in the quality of compressions. This change should be made during any intervention associated with appropriate interruption in chest compressions (for example during defibrillation). All efforts should be made to make the exchange in less than five seconds. The anesthesiologist should avoid interruptions as much as possible and try to limit then to no more than ten seconds.
In this new guideline a change in the order of beginning CPR is emphasized recommending chest compression before ventilation (C-A-B instead of A-B-C). This change reflects the growing evidence of the importance of chest compressions. The second step after high-quality chest compressions begins with opening the airways, which can be performed by hyperestension the neck (head tilt-chin lift maneuver) when evidence of cranial or cervical trauma is lacking. Between 0.12% and 3.7% of trauma victims have spinal cord injury 17,19, and the risk is increased in patients with craniofacial trauma 20,21, or Glasgow coma scale < 8 22,23, or both 21,22. If the anesthesiologist suspects a cervical spine injury he should open the airways by the anteriorization of the mandible without hyperextending the neck (jaw trust maneuver) 24; however, if this maneuver is ineffective he should perform the head tilt-chin lift maneuver.
Many of the recommendations for ventilation process contained in the 2005 Guidelines were maintained. During CPR, the primary objective of assisted ventilation is to maintain adequate oxygenation, while the secondary objective is the elimination of CO2. Each ventilation should be performed during one second with a sufficient tidal volume to promote visible thoracic expansion 25. During CPR the cardiac output is approximately 25% to 33% of normal; thus, oxygen and CO2 exchange by the lungs is reduced. As a consequence, low minute volume (lower than the normal tidal volume and respiratory rate) can maintain effective oxygenation and ventilation 25-28. For this reason, during CPR in adults, a tidal volume of approximately 500 to 600 mL (6 to 7 mL.kg-1) is enough 29-31. Excessive ventilation is unnecessary and should be avoided as it causes gastric distension, resulting in complications, such as regurgitation and bronchoaspiration 32-34. More important, by increasing intrathoracic pressure, decreasing venous return, and reducing cardiac output and survival, it can be harmful 34. However, there is insufficient research available recommending the ideal tidal volumes, respiratory rate, or fraction of inspired oxygen during resuscitation.
During the first few minutes of a cardiac arrest in ventricular fibrillation (VF), ventilations are not as important as chest compressions 35-37, since the oxygen in the arterial blood of the patient in cardiorespiratory arrest remains unchanged until the beginning of CPR; then, partial oxygen pressure remains adequate during several minutes of resuscitation. In victims of prolonged cardiac arrest, ventilation and chest compressions are equally important because arterial oxygen is reduced and alveolar pressure of oxygen is insufficient. Ventilation and chest compression are also equally important in patients with cardiac arrest due to asphyxia, drowning, or children in situations of hypoxia 38,39.
The routine use of cricoid cartilage compression during ventilations is not recommended. Seven randomized, controlled studies have demonstrated that cricoid pressure can delay or avoid the correct placement of an advanced airway device and aspiration can be performed despite of this maneuver 40-46.
Rescuers attending an episode of intrahospital CPR and who have rapid access to a defibrillator should first perform CPR immediately and, as soon as possible, defibrillation. This recommendation is made to reinforce early CPR and defibrillation. When ventricular fibrillation is present for more than a few minutes oxygen and metabolic substrates are depleted. A short period of chest compressions can provide oxygen and energy substrates, increasing the likelihood of a successful defibrillation with return of spontaneous circulation 47. However, there is not enough evidence supporting or refuting CPR before defibrillation. In monitored patients the time between the diagnosis of VF and defibrillation should be lower than three minutes. When two or more rescuers are present, one starts CPR while the other arranges and prepares the defibrillator.
Recent human studies 48,49 demonstrated significant survival in patients submitted to a single shock when compared to the use of three shocks and, therefore, the recommendation of a single shock followed by CPR is maintained. The first shock efficacy of biphasic defibrillator is comparable to or better than three shocks of monophasic defibrillator. The consensus for the use of the monophasic defibrillator includes the use of 360 J in all shocks. The biphasic defibrillator should be charged according to the recommendations of the manufacturer (120 to 200 J). If this guidance is unknown the maximal charge should be used.
In pediatric patients data in the literature are insufficient to prove the minimum or maximum safe effective charge. The initial dose of 2 J.kg-1 for the monophasic defibrillator has been proven to be effective for reversion in 18% to 50% of VF 50-52 and when a similar charge is used in a biphasic defibrillator it is successful in 48% of the times 52. However, even with high energy (above 9 J.kg), defibrillation is successful without evidence of adverse events 53-56. Thus, for pediatric patients the use of an initial dose of 2 to 4 J.kg-1 is acceptable. Subsequent defibrillations should have a maximal charge of 4 J.kg-1 and an increase in energy can be considered, never exceeding 10 J.kg-1 or the maximum adult dose.
Evidence demonstrate that the four placements of electrodes for defibrillation (anterolateral, anteroposterior, left-anterior and infrascapular, and right-anterior and infrascapular) 57 are equally effective in the treatment of atrial or ventricular arrhythmias 58-62. Any one of the four positions can be used for defibrillation; however, to facilitate orientation and training, the anterolateral position should be used.
In patients with implantable cardioverter-defibrillator (ICD) or pacemaker, the device has the potential of malfunctioning after defibrillation when the paddles are placed close to the device 63,64. A study with a cardioverter 63 demonstrated that the paddles for defibrillation should be at least 8 cm from the cardioverter to prevent changes in function of the ICD or pacemaker. The anteroposterior and anterolateral positions are acceptable and avoiding placing the paddles on the device to prevent delaying the defibrillation process is recommended.
ADVANCED LIFE SUPPORT
To treat cardiac arrest, interventions for advanced life support should be preceded by adequate basic life support with early recognition and activation of the emergency response team, and rapid CPR and defibrillation to increase the probability of return of spontaneous circulation (ROSC) with pharmacologic therapy and the use of advanced airway monitoring devices. After ROSC, survival and neurological outcome can be improved with specific and systematic post-cardiac arrest care in the ICU with the use of therapeutic hypothermia and reduction of the fraction of inspired oxygen, using the lower level to obtain an arterial oxygen saturation of 94%.
According to the new 2010 guidelines, some key recommendations were added. The use of capnography and capnometry during the peri-CPR period is recommended to confirm tracheal intubation and follow-up the quality of chest compressions. The algorithm has been simplified to emphasize the importance of quality CPR. Atropine is no longer recommended as routine treatment for patients with pulseless electrical activity (PEA) or asystole.
Airway management and ventilation
The ideal level of the fraction of inspired oxygen (FiO2) to be used during the ventilation process of a patient in CRA is not known. Although prolonged exposure to FiO2 of 100% is potentially toxic, evidence indicating such occurrence in patients submitted to this exposure for a short period of time during CPR is lacking 65-67. The empirical use of FiO2 of 100% during CPR optimizing arterial oxygen concentration, therefore increa sing O2 delivery, is recommended.
All health care professionals should be trained and qualified to use the bag-valve-mask device during ventilations 68,69. However, this is not recommended when the professional administers CPR alone and, in this case, mouth-to-mouth or mouth-to-mask is more efficient. When a second rescuer is available, the bag-valve-mask device can be used as long as he has been trained and has experience with this device. The adult bag (1 to 2 L) should be used, delivering a tidal volume of approximately 600 mL, which is enough to promote thoracic expansion for one second 30.
Because the upper airway obstruction is secondary to the fall of the tongue, the use of oropharyngeal cannula can improve ventilation. Although studies do not consider specifically the use of the oropharyngeal cannula in patients in CRA, and incorrect placement of this device could worsen the obstruction due to tongue dislocation to the postero-inferior region, the use of this device is recommended in unconscious patients by trained personnel.
The cost-benefit of obtaining an advanced airway should be evaluated during CPR. There are not enough studies indicating the ideal moment for this purpose. In a record of 25,006 intra-hospital CPRs, securing advanced airway early (< five minutes) was not associated with an increase in the return of spontaneous circulation, but it was associated with increased 24-hour survival 70.
Tracheal intubation was considered the optimal method of airways management in patients in CRA. The tracheal tube keeps the airways patent and allow aspiration of secretions, ventilation with elevated FiO2, refined tidal volume adjustments, and an alternative to the administration of specific drugs. Note that with the balloon it is possible to protect the airways against aspirations. Although intubation can be performed during chest compressions, it is often associated with interruptions of compressions for several seconds. The use of supraglottic devices represents an alternative to tracheal intubation, being recommended in this new guideline. When compared to the face mask, the laryngeal mask (LM) promotes more safe and reliable ventilation 71,72. Although LM does not guarantee absolute protection against aspiration, studies have revealed that regurgitation is lower with LM than with the face mask, and aspiration is uncommon. Compared to the tracheal tube, LM promotes equivalent ventilation 72,73, and the reported success rate of ventilation during CPR ranges from 72% to 97% of patients 74,75. For qualified health care professionals the use of the LM is an acceptable alternative to bag-valve-mask ventilation or tracheal intubation for airway management of patients in cardiac arrest.
Once the advanced device has been inserted in the airway it should be evaluated to guarantee the correct positioning. In a retrospective study tracheal intubation was associated with an incidence of 6% to 25% of undiagnosed incorrect positioning or dislocation of the tube 76. This assessment will be done during CPR maneuvers through the physical exam (bilateral chest expansion, and lung and epigastric auscultation), besides identification of expired CO2 and capnography curves. Studies with capnography to determine the tracheal tube placement in patients in CRA have shown 100% sensitivity and specificity for the correct diagnosis 76,77. Thereafter, ventilations and compressions will be performed uninterruptedly (eight to ten ventilations.minute-1 and one hundred compressions.minute-1) unless ventilation is inadequate when compressions are not interrupted.
Cardiac arrest management
Cardiac arrests are associated with four different rhythms: ventricular fibrillation (VF), pulseless ventricular tachycardia (PVT), pulseless electrical activity (PEA), and asystole. Ventricular fibrillation represents a disorganized electrical activity, while PVT is an organized electrical activity, both without the ability to generate blood flow. Pulseless electrical activity comprehends a heterogeneous group of organized electrical rhythm associated with the absence or ineffectiveness of ventricular mechanical activity. Asystole represents the absence of detectable electrical ventricular activity. Figure 2 shows the complete algorithm of the advanced life support.
Understanding the importance of the diagnosis and treatment of the underline cause is fundamental for the management of all rhythms associated with cardiac arrest. During CPR, one should consider the "Hs" and "Ts" to identify and treat the factors responsible for the arrest or that are hindering a successful resuscitation (Table I).
Ventricular fibrillation and pulseless ventricular tachycardia
Whenever the diagnosis of VF or PVT is made, one should start immediately chest compressions while a second rescuer charges the defibrillator. The time interval without CPR for defibrillation should be as short as possible with synchronized team work. If a biphasic defibrillator is available the charge indicated by the manufacturer (120 or 200 J), or the maximum charge, should be used. In case of a monophasic defibrillator, a charge of 360 J should be used. After the shock, chest compressions should resume (without verifying rhythm or pulse) for two minutes. After this period the sequence is repeated beginning by checking the rhythm.
A precordial thump should be considered only on monitored unstable ventricular tachycardia and when a defibrillator is not available, and it should not delay the onset of CPR and defibrillation.
Whenever VF or PVT persists after the first shock and after two minutes of CPR it is possible to use a vasopressor to increase myocardial blood flow. The maximal effect of a bolus of intravenous (IV) / intraosseous (IO) vasopressor agent is one to two minutes. If the shock fails to reverse the rhythm, a vasopressor should be used to optimize the potential impact of increased myocardial blood flow before the next defibrillation. However, if the shock results in a rhythm that generates a pulse the dose of vasopressor administered before checking the rhythm and pulse can in theory generate a harmful effect in cardiovascular stability. This complication can be avoided by using continuous monitoring, such as capnography, invasive blood pressure, and central venous saturation for the early detection of the return of spontaneous circulation (ROSC) during chest compressions 78-80. After the shock, pauses to verify the rhythm and pulse should be added; before the administration of the vasopressor, reducing myocardial perfusion during a critical period after the shock can reduce the chances of ROSC.
It has been clinically proven that amiodarone is the first line antiarrhythmic drug in cardiac arrest, since it increases the rate of ROSC. It is indicate in patients with VF/PVT unresponsive to CPR, defibrillation, and vasopressors. If amiodarone is not available, one might consider lidocaine; however, clinical studies did not show increase in the rate of ROSC with lidocaine when compared to amiodarone.
Diagnosis and treatment of the causative factors of VF/PVT are fundamental for the correct management of all rhythms of CRA. Anesthesiologists should not forget the 5 Hs and 5 Ts to identify the causes of CRA or factor that may be complicating the process of resuscitation.
Pulseless electrical activity and asystole
When verifying the rhythm of cardiac arrest and there is no indication for electrical shock, chest compressions should be immediately initiated and continued for two minutes until a new verification of the rhythm. When this rhythm is organized, one should check the pulse. If a pulse is present, post-cardiac arrest care should be immediately initiated.
A vasopressor should be administered as soon as possible to increase myocardial and cerebral blood flow during CPR and to achieve ROSC. Available evidence suggests that routine use of atropine during PEA or asystole has no benefits.
For this reason, atropine was removed from the new CPR guidelines.
Frequently, pulseless electrical activity is caused by reversible conditions that can be successfully treated if they are correctly identified. During the two minutes of chest compressions, anesthesiologists should remember the 5 Hs and 5 Ts (Table I) that could have led to CPR and correct them.
Asystole is frequently a final rhythm after prolonged VF or PEA and, therefore, the prognosis is frequently very poor.
Monitoring during CPR
According to the new 2010 guidelines, there is greater emphasis on physiologic monitoring to optimize the quality of CPR and for early detection of ROSC. Animal and human studies indicate that following-up the expired fraction of CO2 (ETCO2), coronary perfusion pressure (CPP), and central venous oxygen saturation (SvcO2) provide useful information on CPR and patient's response to treatment. In addition, a sudden increase in any of these parameters is a sensitive indicator of ROSC, which can be monitored without interrupting chest compressions 80,81.
Although it is common practice, studies validating pulse palpation during CPR are lacking. The inferior vena cava does not have valves, and the retrograde blood flow during CPR can produce pulsations in the femoral vein 82. Carotid pulse during CPR does not show the efficacy of myocardial or cerebral perfusion.
The use of continuous capnography and capnometry during the peri-CPR period is a formal recommendation. With constant ventilation, ETCO2 has good correlation with cardiac output during CPR. This correlation could be altered with the administration of intravenous sodium bicarbonate 83. This is due to the fact that bicarbonate is converted into CO2 and water, causing a transient increase in the elimination of CO2 by the lungs, and this change should not be mistakenly interpreted as a sign of ROSC. On the other hand, administration of vasopressor causes a transient reduction in ETCO2 due to the increase in afterload and reduction in cardiac output, which should not be interpreted as a reduction in the quality of CPR 84. The presence of persistently low ETCO2 (< 10 mmHg) during CPR in intubated patients suggests that ROSC is unlikely 78,85. A study showed that low values of ETCO2 in nonintubated patients during CPR are not a reliable predictor to achieve ROSC 86. Leaks during ventilation with a face mask or supraglottic device may result in low ETCO2. If ETCO2 is < 10 mmHg in patients being ventilated without leaks, one should improve the quality of CPR with optimization of chest compressions. If a sudden increase in ETCO2 to normal levels (35 to 40 mmHg) is observed, it should be considered an indication of ROSC.
Coronary perfusion pressure (aortic diastolic pressure - right atrial diastolic pressure) during CPR correlates with myocardial blood flow and ROSC 87. A study in humans revealed that ROSC is related with a CPP > 15 mmHg during CPR 88. The specific target for diastolic blood pressure to optimize the chances of ROSC has not been established. Diastolic blood pressure should be used in monitoring the quality of CPR, optimizing chest compressions and guiding vasopressor therapy. If diastolic blood pressure is < 20 mmHg, one should attempt to improve the quality of compressions with vasopressor, or both. Invasive blood pressure monitoring may also be used in the early detection of ROSC during chest compressions.
Patients being monitored with continuous SvcO2 show during CPR levels of 25% to 35% (normal of 60% to 80%) revealing inadequate blood flow. In a clinical study, the presence of SvcO2 < 30% during CPR was associated with lack of successful ROSC 89. For this reason, if SvcO2 is lower than 30%, improving resuscitation maneuvers is recommended.
The use of echocardiogram during cardiac arrest has not been specifically investigated regarding its impact on the outcome. However, some studies suggest that transthoracic and transesophageal echocardiogram is potentially useful in the diagnosis and treatment of the causes of cardiac arrest, such as cardiac tamponade, pulmonary embolism, ischemia, and dissection of the aorta 90-92.
The primary objective of pharmacologic therapy during cardiac arrest is to facilitate recovery and maintenance of spontaneous rhythm with perfusion. With this objective the use of drugs is associated with an increase in ROSC, but not with an increase in long-term survival with good neurologic outcome.
Adrenaline has beneficial effects in patients in cardiac arrest by stimulating alpha-adrenergic receptors, and increasing coronary perfusion pressure and cerebral perfusion pressure 93,94. The dose of 1 mg EV/IO is administered every three to five minutes during CPR. Higher doses may be used when indicated to treat specific problems, such as overdose of beta blockers or calcium channel blockers, or when invasive hemodynamic monitoring is available. If intravenous or intraosseous access is not available, 2 to 2.5 mg of adrenaline may be administered endotracheally, followed by 10 mL of sterile saline.
Randomized clinical assays and metanalysis did not demonstrate differences in the results (ROSC, survival, and neurologic outcome) with the use of 40 U of IV vasopressin versus 1 mg of IV adrenaline 95. For this reason, a dose of 40 U of IV/IO vasopressin can substitute the first or second dose of adrenaline in the treatment of cardiac arrest.
Evidence that any antiarrhythmic medication administered routinely during cardiac arrest increases survival is lacking. However, it has been demonstrated that amiodarone increases short-term survival when compared to placebo or lidocaine, and its use should be considered in cases of VF/PVT unresponsive to CPR, defibrillation, and vasopressor therapy at an initial dose of 300 mg IV/IO followed by a dose of 150 mg IV/IO, if needed. There is no evidence that supports the use of lidocaine in patients with refractory VF/PVT, and it should only be used in the absence of amiodarone at an initial dose of 1.0 to 1.5 mg.kg-1 IV and additional doses of 0.5 to 0.75 mg.kg-1 IV with ten-minute intervals and a maximal dose of 3 mg.kg-1. Magnesium sulfate in cardiac arrest is not routinely recommended, but only in the presence of torsades de pointes at a dose of 1 to 2 g IV/IO diluted in 10 mL of D5W.
Clinical studies have demonstrated conflicting evidence regarding the benefits of the routine use of atropine in cardiac arrest 96,97. For this reason atropine was removed from the asystole and PVT protocol in this last review.
It has been observed that sodium bicarbonate during cardiac arrest is related to a series of adverse events, compromising coronary perfusion pressure by reducing systemic vascular resistance 98. Furthermore, it promotes extracellular alkalosis, hypernatremia, excess of CO2, and paradoxal intracellular acidosis 99. In special resuscitation situations, such as preexisting metabolic acidosis, hyperkalemia, or overdoses with tricyclic antidepressants, bicarbonate may be beneficial. However, the routine use of bicarbonate in patients in cardiac arrest is not recommended. Thus, for lack of evidence, calcium is not recommended in CPR 100.
In cardiac arrests, high-quality cardiopulmonary resuscitation is fundamental for the successful return of spontaneous circulation. During resuscitation, frequent chest compression of adequate depth allowing the complete recoil of the thorax after each compression, minimizing interruptions and avoiding excessive ventilation should be the goals. The quality of CPR should be continuously monitored to optimize resuscitation efforts and early recognition of the return of spontaneous circulation. We hope that this update of the new CPR guidelines improves the quality of resuscitation and survival of patients in cardiac arrest.
1. Stiell IG, Wells GA, Field B et al. - Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med, 2004;351:647-656. [ Links ]
2. Chan RPC, Auler Jr JOC - Estudo restrospectivo da incidência de óbitos anestésico-cirúrgicos nas primeiras 24 horas. Revisão de 82.641 anestesias. Rev Bras Anestesiol, 2002;52:719-727. [ Links ]
3. Pedersen T - Complications and death following anaesthesia. Aprospective study with special reference to the influence of patient-anaesthesia and surgery-related risk factors. Dan Med Bull, 1994;41:319-331. [ Links ]
4. Braz LG, Braz JRC, Módolo NSP et al. - Incidência de parada cardíaca durante anestesia, em hospital universitário de atendimento terciário. Estudo prospectivo entre 1996 e 2002. Rev Bras Anestesiol, 2004;54(6):755-768. [ Links ]
5. Timerman S, Gonzalez MMC, Ramires JAF et al. - Rumo ao consenso internacional de ressuscitação cardiopulmonar e cuidados cardiovasculares de emergência 2010 da Aliança Internacional dos Comitês de Ressuscitação. Rev Bras Clin Med, 2010;8(3):228-37. [ Links ]
6. Berg RA, Hemphill R, Abella BS et al. - Adult Basic life support. 2010 American Heart Association guidelines for cardiopulmonary ressuscitation and emergency cardiovascular care. Circulation, 2010;122(suppl 3):S685-S705. [ Links ]
7. Christenson J, Andrusiek D, Everson-Stewart S et al. - Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation, 2009;120:1241-1247. [ Links ]
8. Berdowski J, Beekhuis F, Zwinderman AH et al. - Importance of the first link: description and recognition of an out-ofhospitalcardiac arrest in an emergency call. Circulation, 2009;119:2096-2102. [ Links ]
9. Lapostolle F, Le Toumelin P, Agostinucci JM et al. - Basic cardiac life support providers checking the carotid pulse: performance, degree of conviction, and influencing factors. Acad Emerg Med, 2004;11:878- 880. [ Links ]
10. Ochoa FJ, Ramalle-Gomara E, Carpintero JM et al. - Competence of health professionals to check the carotid pulse. Resuscitation, 1998;37:173-175. [ Links ]
11. Olasveengen TM, Wik L, Steen PA - Standard basic life support vs. continuous chest compressions only in out-of-hospital cardiac arrest. Acta Anaesthesiol Scand, 2008;52:914-919. [ Links ]
12. Ong ME, Ng FS, Anushia P et al. - Comparison of chest compression only and standard cardiopulmonary resuscitation for out-of-hospital cardiac arrest in Singapore. Resuscitation, 2008;78:119-126. [ Links ]
13. Bohm K, Rosenqvist M, Herlitz J et al. - Survival is similar after standard treatment and chest compression only in out-ofhospital bystander cardiopulmonary resuscitation. Circulation, 2007;116:2908-2912. [ Links ]
14. Sugerman NT, Edelson DP, Leary M et al. - Rescuer fatigue during actual in-hospital cardiopulmonary resuscitation with audiovisual feedback: a prospective multicenter study. Resuscitation, 2009;80:981-984. [ Links ]
15. Manders S, Geijsel FE - Alternating providers during continuous chest compressions for cardiac arrest: every minute or every two minutes? Resuscitation, 2009;80:1015-1018. [ Links ]
16. Heidenreich JW, Berg RA, Higdon TA et al. - Rescuer fatigue: standard versus continuous chest-compression cardiopulmonary resuscitation. Acad Emerg Med, 2006;13:1020-1026. [ Links ]
17. Rhee P, Kuncir EJ, Johnson L et al. - Cervical spine injury is highly dependent on the mechanism of injury following blunt and penetrating assault. J Trauma, 2006;61:1166-1170. [ Links ]
18. Lowery DW, Wald MM, Browne BJ et al. - Epidemiology of cervical spine injury victims. Ann Emerg Med, 2001;38:12-16. [ Links ]
19. Milby AH, Halpern CH, Guo W et al. - Prevalence of cervical spinal injury in trauma. Neurosurg Focus, 2008;25:E10. [ Links ]
20. Mithani SK, St-Hilaire H, Brooke BS et al. - Predictable patterns of intracranial and cervical spine injury in craniomaxillofacial trauma: analysis of 4786 patients. Plast Reconstr Surg, 2009;123:1293-1301. [ Links ]
21. Hackl W, Hausberger K, Sailer R et al. - Prevalence of cervical spine injuries in patients with facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2001;92:370-376. [ Links ]
22. Holly LT, Kelly DF, Counelis GJ et al. - Cervical spine trauma associated with moderate and severe head injury: incidence, risk factors, and injury characteristics. J Neurosurg Spine, 2002;96:285-291. [ Links ]
23. Demetriades D, Charalambides K, Chahwan S et al. - Nonskeletal cervical spine injuries: epidemiology and diagnostic pitfalls. J Trauma, 2000;48:724-727. [ Links ]
24. Rhee P, Kuncir EJ, Johnson L et al. - Cervical spine injury is highly dependent on the mechanism of injury following blunt and penetrating assault. J Trauma, 2006;61:1166-1170. [ Links ]
25. Baskett P, Nolan J, Parr M - Tidal volumes which are perceived to be adequate for resuscitation. Resuscitation, 1996;31:231-234. [ Links ]
26. Berg RA, Kern KB, Hilwig RW et al. - Assisted ventilation does not improve outcome in a porcine model of single-rescuer bystander cardiopulmonary resuscitation. Circulation, 1997;95:1635-1641. [ Links ]
27. Berg RA, Kern KB, Hilwig RW et al. - Assisted ventilation during 'bystander' CPR in a swine acute myocardial infarction model does not improve outcome. Circulation, 1997;96:4364-4371. [ Links ]
28. Tang W, Weil MH, Sun S et al. - Cardiopulmonary resuscitation by precordial compression but without mechanical ventilation. Am J Respir Crit Care Med, 1994;150(6 pt 1):1709-1713. [ Links ]
29. Wenzel V, Keller C, Idris AH et al. - Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk? Resuscitation, 1999;43:25-29. [ Links ]
30. Dorges V, Ocker H, Hagelberg S et al. - Smaller tidal volumes with room-air are not sufficient to ensure adequate oxygenation during bag-valve-mask ventilation. Resuscitation, 2000;44:37-41. [ Links ]
31. Dorges V, Ocker H, Hagelberg S et al. - Optimisation of tidal volumes given with self-inflatable bags without additional oxygen. Resuscitation, 2000;43:195-199. [ Links ]
32. Berg MD, Idris AH, Berg RA - Severe ventilatory compromise due to gastric distention during pediatric cardiopulmonary resuscitation. Resuscitation, 1998;36:71-73. [ Links ]
33. Garnett AR, Ornato JP, Gonzalez ER et al. - End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA, 1987;257:512-515. [ Links ]
34. Aufderheide TP, Sigurdsson G, Pirrallo RG et al.- Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation, 2004;109:1960-1965. [ Links ]
35. Sayre MR, Berg RA, Cave DM et al. - Hands-only (compressiononly) cardiopulmonary resuscitation: a call to action for bystander response to adults who experience out-of-hospital sudden cardiac arrest: a science advisory for the public from the American Heart Association Emergency Cardiovascular Care Committee. Circulation, 2008;117:2162-2167. [ Links ]
36. Berg RA, Sanders AB, Kern KB et al. - Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation, 2001;104:2465-2470. [ Links ]
37. Kern KB, Hilwig RW, Berg RA et al. - Importance of continuous chest compressions during cardiopulmonary resuscitation: improved outcome during a simulated single lay-rescuer scenario. Circulation, 2002;105:645-649. [ Links ]
38. Kitamura T, Iwami T, Kawamura T et al. - Conventional and chestcompression- only cardiopulmonary resuscitation by bystanders for children who have out-of-hospital cardiac arrests: a prospective, nationwide, population-based cohort study, Lancet. 2010. [ Links ]
39. Berg RA, Hilwig RW, Kern KB et al. - "Bystander" chest compressions and assisted ventilation independently improve outcome from piglet asphyxial pulseless "cardiac arrest." Circulation, 2000;101:1743-1748. [ Links ]
40. McNelis U, Syndercombe A, Harper I et al. - The effect of cricoid pressure on intubation facilitated by the gum elastic bougie. Anaesthesia, 2007;62:456-459. [ Links ]
41. Harry RM, Nolan JP - The use of cricoid pressure with the intubating laryngeal mask. Anaesthesia, 1999;54:656-659. [ Links ]
42. Noguchi T, Koga K, Shiga Y et al. - The gum elastic bougieeases tracheal intubation while applying cricoid pressure compared to a stylet. Can J Anaesth, 2003;50:712-717. [ Links ]
43. Asai T, Murao K, Shingu K - Cricoid pressure applied after placement of laryngeal mask impedes subsequent fibreoptic tracheal intubation through mask. Br J Anaesth, 2000;85:256-261. [ Links ]
44. Snider DD, Clarke D, Finucane BT - The "BURP" maneuver worsens the glottic view when applied in combination with cricoid pressure. Can J Anaesth, 2005;52:100-104. [ Links ]
45. Smith CE, Boyer D - Cricoid pressure decreases ease of tracheal intubation using fibreoptic laryngoscopy (WuScope System). Can J Anaesth, 2002;49:614-619. [ Links ]
46. Asai T, Barclay K, Power I et al. - Cricoid pressure impedes placement of the laryngeal mask airway and subsequent tracheal intubation through the mask. Br J Anaesth, 1994;72:47-51. [ Links ]
47. Eftestol T, Wik L, Sunde K et al. - Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest. Circulation, 2004;110:10-15. [ Links ]
48. Bobrow BJ, Clark LL, Ewy GA et al. - Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. JAMA, 2008;299:1158-1165. [ Links ]
49. Rea TD, Helbock M, Perry S et al. - Increasing use of cardiopulmonary resuscitation during out-ofhospital ventricular fibrillation arrest: survival implications of guideline changes. Circulation, 2006;114:2760-2765. [ Links ]
50. Berg MD, Samson RA, Meyer RJ et al. - Pediatric defibrillation doses often fail to terminate prolonged out-ofhospital ventricular fibrillation in children. Resuscitation, 2005;67:63-67. [ Links ]
51. Rodriguez-Nunez A, Lopez-Herce J, Garcia C et al. - Pediatric defibrillation after cardiac arrest: initial response and outcome. Crit Care, 2006;10:R113. [ Links ]
52. Tibballs J, Carter B, Kiraly NJ et al. - External and internal biphasic direct current shock doses for pediatric ventricular fibrillation and pulseless ventricular tachycardia. Pediatr Crit Care Med, 2011;12(1):14-20. [ Links ]
53. Atkins DL, Hartley LL, York DK - Accurate recognition and effective treatment of ventricular fibrillation by automated external defibrillators in adolescents. Pediatrics, 1998;101:393-397. [ Links ]
54. Rossano JW, Quan L, Kenney MA et al. - Energy doses for treatment of out-of-hospital pediatric ventricular fibrillation. Resuscitation, 2006;70:80-89. [ Links ]
55. Gurnett CA, Atkins DL - Successful use of a biphasic waveform automated external defibrillator in a high-risk child. Am J Cardiol, 2000;86:1051-1053. [ Links ]
56. Atkins DL, Jorgenson DB - Attenuated pediatric electrode pads for automated external defibrillator use in children. Resuscitation, 2005;66:31-37. [ Links ]
57. England H, Hoffman C, Hodgman T et al. - Effectiveness of automated external defibrillators in high schools in greater Boston. Am J Cardiol, 2005;95:1484-1486. [ Links ]
58. Boodhoo L, Mitchell AR, Bordoli G et al. - Cardioversion of persistent atrial fibrillation: a comparison of two protocols. Int J Cardiol, 2007;114:16-21. [ Links ]
59. Brazdzionyte J, Babarskiene RM, Stanaitiene G - Anterior-posterior versus anterior-lateral electrode position for biphasic cardioversion of atrial fibrillation. Medicina (Kaunas), 2006;42:994-998. [ Links ]
60. Chen CJ, Guo GB - External cardioversion in patients with persistent atrial fibrillation: a reappraisal of the effects of electrode pad position and transthoracic impedance on cardioversion success. Jpn Heart J, 2003;44:921-932. [ Links ]
61. Stanaitiene G, Babarskiene RM - [Impact of electrical shock waveform and paddle positions on efficacy of direct current cardioversion for atrial fibrillation]. Medicina (Kaunas), 2008;44:665-672. [ Links ]
62. Krasteva V, Matveev M, Mudrov N et al. - Transthoracic impedance study with large self-adhesive electrodes in two conventional positions for defibrillation. Physiol Meas, 2006;27:1009-1022. [ Links ]
63. Manegold JC, Israel CW, Ehrlich JR et al. - External cardioversion of atrial fibrillation in patients with implanted pacemaker or cardioverterdefibrillator systems: a randomized comparison of monophasic and biphasic shock energy application. Eur Heart J, 2007;28:1731-1738. [ Links ]
64. Alferness CA - Pacemaker damage due to external countershock in patients with implanted cardiac pacemakers. Pacing Clin Electrophysiol, 1982;5:457-458. [ Links ]
65. Liu Y, Rosenthal RE, Haywood Y et al. - Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome. Stroke, 1998;29:1679-1686. [ Links ]
66. Zwemer CF, Whitesall SE, D'Alecy LG - Cardiopulmonary-cerebral resuscitation with 100% oxygen exacerbates neurological dysfunction following nine minutes of normothermic cardiac arrest in dogs. Resuscitation, 1994;27:159-170. [ Links ]
67. Lipinski CA, Hicks SD, Callaway CW - Normoxic ventilation during resuscitation and outcome from asphyxial cardiac arrest in rats. Resuscitation, 1999;42:221-229. [ Links ]
68. Bailey AR, Hett DA - The laryngeal mask airway in resuscitation. Resuscitation, 1994;28:107-110. [ Links ]
69. Dorges V, Wenzel V, Knacke P et al. - Comparison of different airway management strategies to ventilate apneic, nonpreoxygenated patients. Crit Care Med, 2003;31:800-804. [ Links ]
70. Wong ML, Carey S, Mader TJ et al. - Time to invasive airway placement and resuscitation outcomes after inhospital cardiopulmonary arrest. Resuscitation, 2010;81:182-186. [ Links ]
71. Stone BJ, Chantler PJ, Baskett PJ - The incidence of regurgitation during cardiopulmonary resuscitation: a comparison between the bag valve mask and laryngeal mask airway. Resuscitation, 1998;38:3-6. [ Links ]
72. [Study group] - The use of the laryngeal mask airway by nurses during cardiopulmonary resuscitation: results of a multicentre trial. Anaesthesia, 1994;49:3-7. [ Links ]
73. Samarkandi AH, Seraj MA, el Dawlatly A et al. - The role of laryngeal mask airway in cardiopulmonary resuscitation. Resuscitation, 1994;28:103-106. [ Links ]
74. Rumball CJ, MacDonald D - The PTL, Combitube, laryngeal mask, and oral airway: a randomized prehospital comparative study of ventilatory device effectiveness and cost-effectiveness in 470 cases of cardiorespiratory arrest. Prehosp Emerg Care, 1997;1:1-10. [ Links ]
75. Tanigawa K, Shigematsu A - Choice of airway devices for 12,020 cases of nontraumatic cardiac arrest in Japan. Prehosp Emerg Care, 1998;2:96-100. [ Links ]
76. Silvestri S, Ralls GA, Krauss B et al. - The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med, 2005;45:497-503. [ Links ]
77. Tong YL, Sun M, Tang WH et al. - The tracheal detecting-bulb: a new device to distinguish tracheal from esophageal intubation. Acta Anaesthesiol Sin, 2002;40:159-163. [ Links ]
78. Kolar M, Krizmaric M, Klemen P et al. - Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care, 2008;12:R115. [ Links ]
79. Grmec S, Mally S - Timeliness of administration of vasopressors in CPR. Crit Care, 2009;13:401. [ Links ]
80. Pokorna M, Necas E, Kratochvil J et al. - A sudden increase in partial pressure end-tidal carbon dioxide (P(ET)CO(2)) at the moment of return of spontaneous circulation. J Emerg Med, 2009;38:614-621. [ Links ]
81. Grmec S, Krizmaric M, Mally S et al. - Utstein style analysis of out-ofhospital cardiac arrest- bystander CPR and end expired carbon dioxide. Resuscitation, 2007;72:404-414. [ Links ]
82. Connick M, Berg RA - Femoral venous pulsations during open-chest cardiac massage. Ann Emerg Med, 1994;24:1176-1179. [ Links ]
83. Okamoto H, Hoka S, Kawasaki T et al. - Changes in end-tidal carbon dioxide tension following sodium bicarbonate administration: correlation with cardiac output and haemoglobin concentration. Acta Anaesthesiol Scand, 1995;39:79-84. [ Links ]
84. Cantineau JP, Merckx P, Lambert Y et al. - Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation. Am J Emerg Med, 1994;12:267-270. [ Links ]
85. Grmec S, Kupnik D - Does the Mainz Emergency Evaluation Scoring (MEES) in combination with capnometry (MEESc) help in the prognosis of outcome from cardiopulmonary resuscitation in a prehospital setting? Resuscitation, 2003;58:89-96. [ Links ]
86. Nakatani K, Yukioka H, Fujimori M et al. - Utility of colorimetric endtidal carbon dioxide detector for monitoring during prehospital cardiopulmonary resuscitation. Am J Emerg Med, 1999;17:203-206. [ Links ]
87. Halperin HR, Tsitlik JE, Gelfand M et al. - A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest. N Engl J Med, 1993;329:762-768. [ Links ]
88. Paradis NA, Martin GB, Rivers EP et al. - Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA, 1990;263:1106-1113. [ Links ]
89. Rivers EP, Martin GB, Smithline H et al. - The clinical implications of continuous central venous oxygen saturation during human CPR. Ann Emerg Med, 1992;21:1094-1101. [ Links ]
90. Memtsoudis SG, Rosenberger P, Loffler M et al. - The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery. Anesth Analg, 2006;102:1653-1657. [ Links ]
91. Niendorff DF, Rassias AJ, Palac R et al. - Rapid cardiac ultrasound of inpatients suffering PEA arrest performed by nonexpert sonographers. Resuscitation, 2005;67:81-87. [ Links ]
92. Tayal VS, Kline JA - Emergency echocardiography to detect pericardial effusion in patients in PEA and near-PEA states. Resuscitation, 2003;59:315-318. [ Links ]
93. Yakaitis RW, Otto CW, Blitt CD - Relative importance of alpha and beta and adrenergic receptors during resuscitation. Crit Care Med, 1979;7:293-296. [ Links ]
94. Michael JR, Guerci AD, Koehler RC et al. - Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. Circulation, 1984;69:822-835. [ Links ]
95. Aung K, Htay T - Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med, 2005;165:17-24. [ Links ]
96. Engdahl J, Bang A, Lindqvist J et al. - Can we define patients with no and those with some chance of survival when found in asystole out of hospital? Am J Cardiol, 2000;86:610-614. [ Links ]
97. Engdahl J, Bang A, Lindqvist J et al. - Factors affecting short- and long-term prognosis among 1069 patients with out-of-hospital cardiac arrest and pulseless electrical activity. Resuscitation, 2001;51:17-25. [ Links ]
98. Kette F, Weil MH, Gazmuri RJ - Buffer solutions may compromise cardiac resuscitation by reducing coronary perfusion presssure. JAMA, 1991;266:2121-2126. [ Links ]
99. Graf H, Leach W, Arieff AI - Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science, 1985;227:754-756. [ Links ]
100. van Walraven C, Stiell IG, Wells GA et al. - Do advanced cardiac life support drugs increase resuscitation rates from in-hospital cardiac arrest? The OTAC Study Group. Ann Emerg Med, 1998;32:544-553. [ Links ]
Correspondence to: Submitted on November 8, 2010. Receives from the Anesthesiology, Pain and Intensive Care Medicine Discipline of the Universidade Federal de São Paulo - Escola Paulista de Medicina (UNIFESP-EPM), Brazil.
Dr. Luiz Fernando dos Reis Falcão
Rua Napoleão de Barros, 715 - 5º andar Vila Clementino
04024-900 - São Paulo, SP, Brazil
Approved on January 31, 2011.
Submitted on November 8, 2010.
Receives from the Anesthesiology, Pain and Intensive Care Medicine Discipline of the Universidade Federal de São Paulo - Escola Paulista de Medicina (UNIFESP-EPM), Brazil.