by Philip J Podrid, MD This is a continuation of the discussion of the guidelines for cardiopulmonary resuscitation. (See "Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-I"). ADVANCED CARDIAC LIFE SUPPORT – Advanced cardiovascular life support (ACLS) includes knowledge and skills necessary to provide appropriate early treatment for cardiopulmonary arrest and includes: • Basic life support, as discussed above • Use of advanced equipment and special techniques for establishing effective ventilation and circulation, including defibrillation; oxygenation, ventilation, and airway control; and devices to assist circulation • ECG monitoring, 12-lead ECG interpretation, and arrhythmia recognition • Establishment and maintenance of intravenous access • Therapies for the treatment of patients with cardiac and respiratory arrest, including postarrest stabilization; this includes adequate knowledge about the antiarrhythmic agents and drugs for optimizing cardiac output and blood pressure ILCOR Universal/International ACLS algorithm – The algorithm developed by the International Liaison Committee on Resuscitation (ILCOR) unifies and simplifies the essential information of adult ACLS (show algorithm 1) [1]. The steps include: • Check responsiveness • Activate EMS response system • Open the airway • Check breathing • Give two effective breaths • Assess circulation • Compress chest, if no signs of circulation detected • If the monitor displays VT or VF or the AED signal and voice prompts are for these arrhythmias, the rescuer should attempt defibrillation up to three times, as necessary. The current recommendation is up to three shocks using energies of 200, 200 to 300, and 360 joules when monophasic waveforms are delivered [2] or an equivalent amount of energy when machines delivering biphasic waveforms are utilized, ie, nonescalating 150 to 170 joules (class IIa recommendation) [3]. If available, a biphasic waveform defibrillator is preferable since the success rate for defibrillation is higher than with monophasic waveforms [4,5]. After three shocks, CPR should be resumed for at least one minute, allowing for a brief period of reoxygenation of blood and circulation of blood to the heart and brain; after this period, the rhythm should be reassessed and repeat shock delivered if appropriate. If VT/VF are refractory to defibrillation, additional interventions are necessary (see below). • If an arrhythmia other than VT or VF, primarily asystole or pulseless electrical activity (PEA), are seen on the monitor or the AED signals "no shock therapy indicated", the responder should immediately check the pulse to determine if the nonshockable rhythm is producing a spontaneous circulation. If no pulse is detected, CPR is initiated and continued for approximately three minutes; the rhythm is then reassessed for the presence of VT or VF or spontaneous return of an organized rhythm in a beating heart. If an organized rhythm is not present, additional interventions are necessary. • Placement and confirmation of a tracheal tube; tube placement is primarily confirmed with physical examination and secondarily with a device that measures end-tidal CO2 or end-diastolic diameter (class IIa recommendation). Oxygenation and ventilation are confirmed with end-tidal CO2 oxygen saturation monitors. The tracheal tube should be secured with special holders (class IIb indication) or tie and tape measures. • Gaining intravenous access and starting an intravenous infusion • Giving appropriate medications, including vasopressin, epinephrine, buffers, or antiarrhythmic drugs [6-13]. Vasopressin has hemodynamic effects that are similar to epinephrine, and some studies have suggested that it produces better outcomes [1,10-13]. However, a triple-blind randomized trial of 200 patients with an in-hospital cardiac arrest found no difference in one hour survival, survival to hospital discharge, and neurologic examination and performance between vasopressin and epinephrine therapy [14]. • Pacing, if indicated • Search for and correction of reversible causes Ventricular fibrillation/pulseless ventricular tachycardia – The algorithm for VF or pulseless VT considered the specifics of the ACLS recommendations for these arrhythmias. Since the ILCOR Universal algorithm assumes that all adult cardiac arrests are due to VF or pulseless VT, the initial part of the algorithm, including basic life support, defibrillation, and therapy of persistent or recurrent VT/VF, is the same and places a strong emphasis on the immediate recognition and treatment of these arrhythmias (show algorithm 4) [1]. • Epinephrine is administered as 1 mg intravenously every three to five minutes; a higher dose (0.2 mg/kg) is acceptable, but not recommended, if the lower dose is ineffective [17,18]. An acceptable alternative is vasopressin, which is recommended only for VT or VF; there is no evidence to support its use in asystole or PEA [1,13,19]. A single intravenous dose of 40 U is given once (since the half life is 10 to 20 minutes compared to 3 to 5 minutes with epinephrine). The potential value of vasopressin was illustrated in a controlled trial of patients with out-of-hospital VF who received either vasopressin or epinephrine; those treated with vasopressin had higher rates of survival to hospital admission (70 versus 35 percent, p = 0.06) and survival at 24 hours (60 versus 20 percent, p = 0.02) [13]. A repeat dose does not appear to be of value and it is uncertain what the best approach is if there is no response. An acceptable approach if there is no response after 5 to 10 minutes is the administration of epinephrine (1 mg every three to five five minutes). • The use of one of the following antiarrhythmic agents is acceptable, although there is only fair evidence supporting their benefit for shock-refractory VT/VF [15,20,21]. - Amiodarone is administered as 300 mg intravenous push. If VF or pulseless VT recurs, the administration of a second 150 mg dose can be considered. The maximum cumulative dose is 2.2 grams over 24 hours [22-26]. - Lidocaine is administered at a dose of 1 to 1.5 mg/kg as an intravenous push. This dose can be repeated every 3 to 5 minutes up a maximum dose of 3 mg/kg [27-30]. - Procainamide, administered at a dose of 30 mg/min intravenously up to a maximum dose of 17 mg/kg is acceptable but not recommended since the prolonged time for administration is unsuitable for a cardiac arrest [29]. - Magnesium sulfate, 1 to 2 grams intravenously is recommended for the treatment of polymorphic VT (torsade de pointes) and suspected hypomagnesemic states [31,32]. • Sodium bicarbonate, 1 meq/kg intravenously, is indicated for severe conditions known to provoke sudden death, such as hyperkalemia, preexisting metabolic acidosis, or certain drug overdoses [8,9]. (See "Pulseless electrical activity" below). Defibrillation, using energy levels discussed above, should be attempted after each medication is administered or after each minute of CPR. Pulseless electrical activity – Pulseless electrical activity (previously called electromechanical dissociation) is defined by the presence of some type of electrical activity other than VT or VF in the absence of a detectable pulse. PEA is often often associated with specific clinical states that can be reversed when identified early and effectively treated (show algorithm 5). Survival is poor when electrical activity is wide and slow; these rhythms often represent the last electrical activity of a dying myocardium or may be associated with hyperkalemia, hypothermia, hypoxia, preexisting acidosis, or a variety of drug overdoses (eg, tricyclic antidepressants, beta blockers, calcium channel blockers, digoxin) (show table 1A-1B). (See "Treatment of hyperkalemia" and see "Basic approach to arrhythmias due to digitalis toxicity"). Electrical activity that is narrow complex and wide indicates a relatively normal heart that is responding as it should; causes include hypovolemia, infection, pulmonary embolism, or cardiac tamponade (show table 1A-1B). (See "Massive pulmonary embolism" and see "Pericardial compressive syndromes"). • It has a class I indication for patient who has known preexisting hyperkalemia. • The use of bicarbonate is acceptable (class IIa indication) when a known, preexisting bicarbonate-responsive acidosis is present; for treatment of tricyclic antidepressant overdose; and to alkalinize the urine in aspirin or other drug overdoses. It is not routinely used for the acute lactic acidosis associated with CPR, but may be given if the initial interventions (defibrillation, ventilation, cardiac compression, and vasopressor therapy) have been ineffective. (See "Bicarbonate therapy in lactic acidosis"). • The use of bicarbonate is acceptable in intubated and ventilated patients with a long arrest interval or upon return of circulation after a long arrest interval; however, there is only fair evidence for its efficacy in these settings. • The use of bicarbonate is harmful and not indicated for respiratory (hypercapnic) acidosis. Asystole – Patients with asystole on a cardiac monitor have a dismal rate of survival, as low as 1 or 2 percent; however, true asystole should be confirmed by checking lead and cable connections, making certain that the monitor is on and that the gain in turned up, and checking another lead for asystole (show algorithm 6). During CPR, brief periods of an organized QRS complex may appear that usually represents an "agonal" rhythm. CPR should not be initiated if the patient has any objective evidence of a do not resuscitate status (DNR) or has any indication that resuscitation attempts are not indicated, eg, signs of death. • Was tracheal intubation performed? • Was effective ventilation achieved? • Was VF, if present, adequately shocked? • Was intravenous access obtained? • Were intravenous epinephrine and atropine given? • Was a reversible cause ruled out or corrected, if identified? • Was asystole continuously documented for more than 5 to 10 minutes after all of the above were accomplished? Bradycardia – Bradycardia may be the cause of cardiac arrest but it is more often associated with signs and symptoms of a low cardiac output (show algorithm 7). These include chest pain, shortness of breath, decreased level of consciousness, low blood pressure, shock, pulmonary congestion, or heart failure. Atropine is effective for treating symptomatic sinus bradycardia (class I recommendation); it may be beneficial in the presence of AV block at the nodal level (class IIa recommendation) or ventricular asystole, but should not be used when infranodal (Mobitz type II block) is suspected. If the patient is symptomatic, atropine is given as the initial drug therapy (0.5 to 1 mg every three to five minutes up to a total of 0.03 to 0.04 mg/kg); however, transcutaneous pacing should not be delayed while awaiting intravenous access or for atropine to take effect (class I indication). Patients who have had a heart transplant and have a denervated heart will not respond to atropine; as a result, pacing and/or catecholamine infusion should be used initially. A transvenous pacemaker should be inserted if second or third degree heart block is present or bradycardia persists after atropine and/or catecholamine infusion; transcutaneous pacing may be used prior to the insertion of a transvenous pacemaker (class I indication). Antiarrhythmic drugs, particularly lidocaine, should not be used in patients with third degree heart block. (See "Third degree (complete) atrioventricular block"). References 1. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: Advanced cardiovascular life support: section 7: algorithm approach to ACLS emergencies: section 7A: principles and practice of ACLS. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102:I136. 2. Weaver, WD, Cobb, LA, Copass, MK, Hallstrom, AP. Ventricular defibrillation: a comparative trial using 175-J and 320-J shocks. N Engl J Med 1982; 307:1101. 3. Cummins, RO, Hazinski, MF, Kerber, RE, et al. Low-energy biphasic waveform defibrillation: evidence-based review applied to emergency cardiovascular care guidelines: a statement for healthcare professionals from the American Heart Association Committee on Emergency Cardiovascular Care and the Subcommittees on Basic Life Support, Advanced Cardiac Life Support, and Pediatric Resuscitation. Circulation 1998; 97:1654. 4. Schneider, T, Martens, PR, Paschen, H, et al, for the Optimal response to Cardiac Arrest (ORCA) Investigators. Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Circulation 2000; 102:1780. 5. Poole, JE, White, RD, Kanz, KG, et al. Low-energy impedance-compensating biphasic waveforms terminate ventricular fibrillation at high rates in victims of out-of-hospital cardiac arrest. J Cardiovasc Electrophysiol 1997; 8:1373. 6. Yakaitis, RW, Otto, CW, Blitt, CD. Relative importance of alpha and beta adrenergic receptors during resuscitation. Crit Care Med 1979; 7:293. 7. 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. 8. Bleske, BE, Rice, TL, Warren, EW, et al. The effect of sodium bicarbonate administration on the vasopressor effect of high-dose epinephrine during cardiopulmonary resuscitation in swine. Am J Emerg Med 1993; 11:439. 9. Neumar, RW, Bircher, NG, Sim, KM, et al. Epinephrine and sodium bicarbonate during CPR following asphyxial cardiac arrest in rats. Resuscitation 1995; 29:249. 10. Strohmenger, HU, Lindner, KH, Prengel, AW, et al. Effects of epinephrine and vasopressin on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation. Resuscitation 1996; 31:65. 11. Prengel, AW, Lindner, KH, Keller, A, Lurie, KG. Cardiovascular function during the postresuscitation phase after cardiac arrest in pigs: a comparison of epinephrine versus vasopressin. Crit Care Med 1996; 24:2014. 12. Morris, DC, Dereczyk, BE, Grzybowski, M, et al. Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation. Acad Emerg Med 1997; 4:878. 13. Lindner, KH, Dirks, B, Strohmenger, HU, et al. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet 1997; 349:535. 14. Stiell, IG, Hebert, PC, Wells, GA, et al. Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial. Lancet 2001; 358:105. 15. 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. 16. Ditchey, RV, Lindenfeld, J. Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs. Circulation 1988; 78:382. 17. Brown, CG, Martin, DR, Pepe, PE, et al. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital [see comments]. N Engl J Med 1992; 327:1051. 18. Gueugniaud, PY, Mols, P, Goldstein, P, et al. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group. N Engl J Med 1998; 339:1595. 19. Lindner, KH, Prengel, AW, Brinkmann, A, et al. Vasopressin administration in refractory cardiac arrest. Ann Intern Med 1996; 124:1061. 20. Redding, JS, Pearson, JW. Resuscitation from ventricular fibrillation: drug therapy. JAMA 1968; 203:255. 21. Stiell, IG, Wells, GA, Hebert, PC, et al. Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs. Acad Emerg Med 1995; 2:264. 22. Helmy, I, Herre, JM, Gee, G, et al. Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias. J Am Coll Cardiol 1988; 12:1015. 23. Kowey, PR, Levine, JH, Herre, JM, et al. Randomized, double-blind comparison of intravenous amiodarone and bretylium in the treatment of patients with recurrent, hemodynamically destabilizing ventricular tachycardia or fibrillation [see comments]. Circulation 1995; 92:3255. 24. Levine, JH, Massumi, A, Scheinman, MM, et al. Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group. J Am Coll Cardiol 1996; 27:67. 25. Scheinman, MM, Levine, JH, Cannom, DS, et al. Dose-ranging study of intravenous amiodarone in patients with life-threatening ventricular tachyarrhythmias [see comments]. Circulation 1995; 92:3264. 26. Kudenchuk, PJ, Cobb, LA, Copass, MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999; 341:871. 27. Armengol, RE, Graff, J, Baerman, JM, Swiryn, S. Lack of effectiveness of lidocaine for sustained, wide QRS complex tachycardia. Ann Emerg Med 1989; 18:254. 28. Nasir, N Jr, Taylor, A, Doyle, TK, Pacifico, A. Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction. Am J Cardiol 1994; 74:1183. 29. Gorgels, AP, van den, Dool A, Hofs, A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol 1996; 78:43. 30. Weaver, WD, Fahrenbruch, CE, Johnson, DD, et al. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990; 82:2027. 31. Tzivoni, D, Banai, S, Schuger, C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation 1988; 77:392. 32. Miller, B, Craddock, L, Hoffenberg, S, et al. Pilot study of intravenous magnesium sulfate in refractory cardiac arrest: safety data and recommendations for future studies. Resuscitation 1995; 30:3.
Basic life support algorithm – The basic life support algorithm, as discussed above includes (show algorithm 2):
Attach defibrillator/monitor – Once the basic life support algorithm is activated, responders should attach a defibrillator and/or monitor to assess the rhythm (show algorithm 3).
Additional interventions – A number of additional interventions are often needed during CPR:
Drug therapy – The use of drugs, including sympathomimetic agents, antiarrhythmic drugs, and buffers has been relegated to a secondary role since there is little evidence that these agents are of benefit; there use is considered indeterminate or class IIb [1,15,16]. (See "Controversies in cardiopulmonary resuscitation" and see "Acute therapy and outcome of sudden cardiac death").
Sodium bicarbonate – Sodium bicarbonate (1 meq/kg) has a role in the treatment of PEA when due to specific causes:
Epinephrine – The efficacy of epinephrine (1 mg intravenous push every three to five minutes) for PEA is uncertain (class indeterminate). If this dose of epinephrine fails, higher doses (up to 0.2 mg/kg) may be used, but are not recommended. There is no evidence to support the routine use of vasopressin for PEA.
Atropine – The administration of atropine (1 mg every three to five minutes) is possibly helpful for PEA when the rate is slow, ie, absolute bradycardia with a rate <60 beats/min or a relative bradycardia (rate less than expected relative to the underlying condition).
Drugs – The indications for the use of sodium bicarbonate, epinephrine, vasopressin, and atropine are the same as discussed above under PEA.
Transcutaneous pacing – Transcutaneous pacing may be effective if performed early and when combined with drug therapy. However, there is no evidence to support the routine use of pacing. (See "Temporary cardiac pacing").
Persistent asystole – When asystole persists, the decision about ceasing further CPR efforts must be made; consideration is given to the quality and duration of CPR.
Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-II
Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-I
by Philip J Podrid, MD UpToDate performs a continuous review of over 270 journals and other resources. Updates are added as important new information is published. The literature review for version 10.3 is current through August 2004; this topic was last changed on August 7, 2004. The outcome of an emergency situation and survival of the patient are critically dependent upon the first few minutes of care; the actions that should occur promptly during this time define basic life support and include [1]: • Prompt recognition and action for myocardial infarction and stroke to prevent respiratory and cardiac arrest • Establishment and maintenance of breathing for victims of respiratory arrest • Attempted cardioversion/defibrillation for patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) with an automated external defibrillator (AED) (show algorithm 1) [2,3]. (See "Basic principles and technique of cardioversion and defibrillation", section on Automatic external cardioverter defibrillator). With the growing availability of AEDs in the community and workplace, basic life support now includes early access to emergency medical services (EMS) system, early cardiopulmonary resuscitation (CPR), and early defibrillation; this is then followed by advanced cardiovascular life support (ACLS) [4,5]. Early access to EMS requires prompt recognition of those emergencies that require time-critical basic life support intervention, most importantly defibrillation. Since most adults with sudden, nontraumatic cardiac arrest have a ventricular tachyarrhythmia, primarily VF, a telephone call to the EMS system should immediately follow recognition of an emergency ("phone first"). Early CPR is the best treatment for cardiac arrest until there is an EMS response, ie, the arrival of ACLS care and an AED [4,5]. Early CPR may prevent VF from deteriorating into asystole, may increase the chance for successful defibrillation, contributes to the preservation of heart and brain function, and significantly improves survival [6,7]. (See "Acute therapy and outcome of sudden cardiac death"). Early defibrillation is the single most important determinant for survival of adult victims of a cardiac arrest [1,3]. Survival from a cardiac arrest caused by VF declines by 7 to 10 percent for each minute without defibrillation; after more than 12 minutes, the survival rate is only 2 to 5 percent [8-13]. Because of the importance of time, the availability of AEDs in the community (public access defibrillation) to be used by trained lay persons is a major advance in CPR. Resuscitation rates with the the AED are as high as 49 percent, which are nearly twice those achieved by successful EMS programs (show algorithm 1) [8,14-18]. Guidelines for basic and advanced cardiovascular life support will be presented here. They are based upon the guidelines published in August 2000 by American Heart Association in collaboration with the International Liaison Committee on Resuscitation [19,20]. Controversies in CPR, such as active compression-decompression CPR, high dose epinephrine, and the need for sodium bicarbonate are also discussed separately. (See "Controversies in cardiopulmonary resuscitation"). SEQUENCE OF BASIC LIFE SUPPORT – The basic life support sequence discussed below applied to victims who are at least eight years of age and includes assessment and support/intervention [19]. No procedures of CPR should be performed until the need has been established by appropriate assessment of initial response, followed by ongoing assessment of the response to CPR (show algorithm 2). Assess responsiveness – After arriving at the side of the collapsed victim, there must be a rapid assessment for any injury and for responsiveness. If neck or head trauma is seen or suspected, the victim should be moved only if absolutely necessary. Activate the EMS system – The EMS system is activated by calling the appropriate local emergency telephone number. Information supplied to the operator includes location of the emergency, telephone number from which the call is being made, the nature of the emergency, the number of persons requiring help, condition of the victim, and what aid is being given; other information may be requested by the operator [21]. Airway – When the victim is unresponsive, it is important to establish if there is spontaneous respiration; to assess breathing, the victim should be supine with an open airway. In the unresponsive victim, muscle tone is decreased and the tongue and epiglottis may obstruct the pharynx [22,23]. The tongue is the most common cause for airway obstruction; moving the lower jaw forward will lift the tongue away from the back of the neck and open the airway. Any visible foreign material or vomitus must be removed from the mouth and liquids or semi-liquids wiped out. Breathing – Once the airway is opened, as assessment for breathing should be performed promptly; the rescuer places his or her ear near the victims mouth and nose while maintaining an open airway. The victim's chest should be observed: • Look for the chest rising and falling • Listen for air escaping during exhalation • Feel for the flow of air The absence of the chest rising and falling and no air being exhaled indicates the absence of respirations. However, even when these signs are present, respiration may be only weak and inadequate; on occasion respiration may be only a reflex, gasping effort or agonal. Absent or inadequate respiration requires rescue breathing while, if respiration is present, the victim should be positioned properly to maintain a patent airway. • The victim should be in as near a true lateral position as possible, with the head dependent to allow free drainage • The position should be stable • Any pressure on the chest that could impair breathing should be avoided • The victim should be easily and safely turned onto the side and returned to the back, if necessary • The position should permit continued observation and access to the airway • The position should not result in injury to the victim; it is important to monitor the lowermost arm for evidence of impaired blood flow [25,26] If the victim remains in the recovery position for more than 30 minutes, he/she should be turned to the opposite side; it is important to avoid injury when turning the victim. • Mouth-to-mouth breathing – Mouth-to-mouth breathing is a quick and efficient way to provide adequate oxygen and ventilation to the victim. The victim's airway is held open by resting the palm of one hand on the victims forehead.; the victim's nose is pinched with the thumb and index finger in order to prevent air from escaping. After the rescuer takes a deep breath, he makes an airtight seal with his/her mouth over the victim's mouth and gives slow breaths, delivering each breath over two seconds, making certain that the victim's chest rises with each breath and feeling air escape during exhalation. After initially delivering two to five breaths, approximately 10 to 12 breaths are delivered each minute, or one every four to five seconds. Gastric inflation often develops during mouth-to-mouth breathing; this risk can be reduced by maintaining an open airway and delivering slow breaths (allowing two seconds between breaths) at the lowest volume that will still make the chest visibly rise with each breath (approximately 700 to 1000 mL) [27,28]. If gastric distension occurs, recheck and open airway and look for the rise an fall of the chest. (see below under complications of rescue breathing). If initial attempts to ventilate the victim are unsuccessful, the victim's head should be repositioned and rescue breathing repeated. On occasion mouth-to-mouth breathing is performed using a barrier device. There are two types of barrier devices: a mouth-to-mask has a one-way valve so that the victim's air does not enter the rescuers mouth; and a face shield, which does not have an exhalation valve and the victim's expired air escapes between the shield and the victim's face. • Mouth-to-nose breathing – The mouth-to-nose method of ventilation is recommended when mouth-to-mouth ventilation is impossible because the mouth cannot be opened (trismus), the mouth is seriously injured, or a tight mouth-to-mouth seal cannot be achieved. The victim's head is tilted back with one hand on the forehead; the other hand is used to lift the victim's mandible (as in the head tilt-chin lift maneuver) and the victim's mouth is closed; the rescuer takes a deep breath, seals his/her lips around the victim's nose. and exhales into the nose. The lips are then removed from the nose, allowing for exhalation; if partial nasal obstruction is present, it may be necessary to open the victim's mouth intermittently to allow for free exhalation. • Bag-to-mouth breathing – Bag-mask devices are often used in the prehospital setting by emergency medical personnel. These devices consist of a self-inflating bag, with a volume of approximately 1600 mL and a nonrebreathing valve attached to a face mask. However, because of difficultly in obtaining a leak-proof seal while both squeezing the bag and maintaining an open airway, these devices are most effective when two trained and experienced rescuers work together, one sealing the mask to the face and the other squeezing the bag over two seconds. When there is only one rescuer, he/she is positioned at the top of the victim's head and the head is tilted back and the mask applied to the victim's face with one hand, using the bridge of the nose as a guide for correct position. The third, fourth, and fifth fingers of the hand are placed along the bony portion of the mandible and the thumb and index finger of the same hand are placed on the mask. The bag is squeezed with the other hand, observing the chest for adequate ventilation; each breath is delivered over two seconds. If gastric distension occurs, slow rescue breathing is continued. There should not be an attempt to expel the stomach contents since this increases the potential for regurgitation. If regurgitation occurs, the victim's entire body is turned to the side, the mouth is wiped out, the body returned to the supine position, and CPR continued. Circulation – Although palpation of the carotid pulse has been the gold standard for determining if the heart is beating, this is not reliable when used by lay persons [40-42]. As a result, the lay person should not rely on the carotid pulse check to determine the need for chest compression or use of an AED. In contrast, the healthcare professional should continue to use the carotid pulse check as one of several signs of circulation; however, many will be unable to identify a carotid pulse within five seconds [42-44]. • Provide initial rescue breathing to the unresponsive, nonbreathing victim. • Look for signs of circulation. With the ear near the victim's mouth look, listen, and feel for normal breathing; quickly scan the victim for any signs of movement. • If the victim is not breathing normally, coughing, or moving, immediately begin chest compression. Healthcare providers should perform a pulse check in conjunction with an assessment for signs of circulation. For victims over one year of age, the carotid artery (located in the groove between the trachea and muscles at the side of the neck) is the preferred artery to palpate. If it is uncertain if circulation is present, chest compression should be initiated immediately. Proper hand placement is established by identifying the lower half of the sternum: • The rescuers fingers are placed on the lower margins of the victims rib cage on the nearest side. • The fingers are slid up the rib cage to the notch where the ribs meet the lower sternum in the center of the lower part of the chest. • The heel of one hand is placed on the lower half of the sternum (not the lowest portion of the sternum, which is the xiphoid process) and the other hand on top of the first, so that the hands are parallel. The long axis of the heel of the hand is placed on the long axis of the sternum; this keeps the main force of compression on the sternum and reduces the chance of rib fracture. • The fingers should be either extended or interlaced, but kept off the chest. Alternatively, the rescuer can achieve correct hand position by placing the heel of the one hand in the center of the chest, between the nipples. Effective chest compression can produce arterial blood pressure peaks of 60 to 80 mmHg, with a mean blood pressure of 40 mmHg; cardiac output resulting from chest compression is probably one-fourth to one-third of normal, but decreases during the course of prolonged CPR [50]. For chest compression to be effective, attention to the following is required: • Elbows locked in position, with the arms straightened and shoulders directly over the hands, so that the thrust of each compression is straight down on the sternum. • In the normal-sized adult, the sternum is compressed approximately 2 inches (4 to 5 cm); however, optimal sternal compression is best gauged by identifying the force that generates a palpable carotid or femoral pulse [51]. • After each compression, the pressure must be completely released, allowing the chest to return to its normal position; the rescuers hands, however, must remain in contact with the victim's sternum to insure proper hand position for subsequent compressions. • The most effective cerebral and coronary perfusion is achieved when 50 percent of the cycle is devoted to chest compression phase and 50 percent to chest relaxation [52,53]. There have been a number of other techniques used in order to improve blood flow during CPR, such as active compression-decompression CPR; however, these methods have not been shown to improve the outcome of CPR. (See "Controversies in cardiopulmonary resuscitation"). Rescue breathing and chest compression should be combined for effective CPR. However, the need for and safety of mouth-to-mouth breathing is an important concern regarding the complexity of CPR and the inexperience of bystanders; in addition there are concerns about the transmission of infectious disease, although the actual risk is very small [54]. Nevertheless, fears regarding disease transmission, especially HIV, are common and result in reluctance to perform mouth-to-mouth ventilation [55-58]. One study evaluated whether chest compression alone was as effective as chest compression and mouth-to-mouth ventilation; the outcome was the same with the two methods [59]. Thus, if a person is unwilling or unable to perform mouth-to-mouth ventilation for an adult victim, chest compression only CPR should be provided rather than no attempt at CPR being made (class IIa recommendation). (See "Controversies in cardiopulmonary resuscitation"). Defibrillation – Most adult victims of sudden, witnessed, nontraumatic cardiac arrest are in ventricular fibrillation. The single most important determinant of survival is the time from collapse to defibrillation; survival from a ventricular fibrillation cardiac arrest declines by 7 to 10 percent for each minute without defibrillation. Early defibrillation in the community is defined as a shock delivered within five minutes of EMS call receipt. Early defibrillation must also be provided in hospitals and medical facilities; in these areas healthcare providers should be able to deliver a shock within three minutes of an arrest (class I recommendation). The discussion of advanced cardiac life support is continued separately. (See "Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-II"). References 1. Cummins, RO, Ornato, JP, Thies, WH, Pepe, PE. Improving survival from sudden cardiac arrest: the "chain of survival" concept: a statement for health professionals from the Advanced Cardiac Life Support Subcommittee and the Emergency Cardiac Care Committee, American Heart Association. Circulation 1991; 83:1832. 2. Calle, PA, Verbeke, A, Vanhaute, O, et al. The effect of semi-automatic external defibrillation by emergency medical technicians on survival after out-of-hospital cardiac arrest: an observational study in urban and rural areas in Belgium. Acta Clin Belg 1997; 52:72. 3. Richless, LK, Schrading, WA, Polana, J, et al. Early defibrillation program: problems encountered in a rural/suburban EMS system. J Emerg Med 1993; 11:127. 4. Larsen, MP, Eisenberg, MS, Cummins, RO, Hallstrom, AP. Predicting survival from out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med 1993; 22:1652. 5. Swor, RA, Jackson, RE, Cynar, M, et al. Bystander CPR, ventricular fibrillation, and survival in witnessed, unmonitored out-of-hospital cardiac arrest. Ann Emerg Med 1995; 25:780. 6. Eisenberg, MS, Hallstrom, AP, Copass, MK, et al. Treatment of ventricular fibrillation. Emergency medical technician defibrillation and paramedic services. JAMA 1984; 251:1723. 7. Weaver, WD, Copass, MK, Bufi, D, et al. Improved neurologic recovery and survival after early defibrillation. Circulation 1984; 69:943. 8. Cummins, RO. From concept to standard-of-care? Review of the clinical experience with automated external defibrillators. Ann Emerg Med 1989; 18:1269. 9. Cummins, RO, Eisenberg, MS. Prehospital cardiopulmonary resuscitation. Is it effective?. JAMA 1985; 253:2408. 10. Cummins, RO, Eisenberg, MS, Hallstrom, AP, Litwin, PE. Survival of out-of-hospital cardiac arrest with early initiation of cardiopulmonary resuscitation. Am J Emerg Med 1985; 3:114. 11. Ladwig, KH, Schoefinius, A, Danner, R, et al. Effects of early defibrillation by ambulance personnel on short- and long-term outcome of cardiac arrest survival: the Munich experiment. Chest 1997; 112:1584. 12. Sweeney, TA, Runge, JW, Gibbs, MA, et al. EMT defibrillation does not increase survival from sudden cardiac death in a two-tiered urban-suburban EMS system. Ann Emerg Med 1998; 31:234. 13. Kellermann, AL, Hackman, BB, Somes, G, et al. Impact of first-responder defibrillation in an urban emergency medical services system. JAMA 1993; 270:1708. 14. O'Rourke, MF, Donaldson, E, Geddes, JS. An airline cardiac arrest program. Circulation 1997; 96:2849. 15. White, RD, Asplin, BR, Bugliosi, TF, Hankins, DG. High discharge survival rate after out-of-hospital ventricular fibrillation with rapid defibrillation by police and paramedics. Ann Emerg Med 1996; 28:480. 16. Davis, EA, Mosesso, VN Jr. Performance of police first responders in utilizing automated external defibrillation on victims of sudden cardiac arrest. Prehosp Emerg Care 1998; 2:101. 17. Mosesso, VN Jr, Davis, EA, Auble, TE, et al. Use of automated external defibrillators by police officers for treatment of out-of-hospital cardiac arrest. Ann Emerg Med 1998; 32:200. 18. White, RD, Hankins, DG, Bugliosi, TF. Seven years' experience with early defibrillation by police and paramedics in an emergency medical services system. Resuscitation 1998; 39:145. 19. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 3: adult basic life support. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102:I22. 20. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 1: Introduction to ACLS 2000: overview of recommended changes in ACLS from the guidelines 2000 conference. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102:I86. 21. Chandra, NC, Hazinski, MF, Stapleton, E. Instructor's Manual for Basic Life Support. American Heart Association, Dallas 1997. 22. Safar, P. Ventilatory efficacy of mouth-to-mouth artificial respiration: airway obstruction during manual and mouth-to-mouth artificial respiration. JAMA 1958; 167:335. 23. Safar, P, Escarraga, LA, Chang, F. Upper airway obstruction in the unconscious patient. J Appl Physiol 1959; 14:760. 24. Handley, AJ, Becker, LB, Allen, M, et al. Single rescuer adult basic life support. An advisory statement from the Basic Life Support Working Group of the International Liaison Committee on Resuscitation (ILCOR). Resuscitation 1997; 34:101. 25. Fulstow, R, Smith, GB. 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Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk?. Resuscitation 1999; 43:25. 31. Bowman, FP, Menegazzi, JJ, Check, BD, Duckett, TM. Lower esophageal sphincter pressure 28. Morton HJV, Wylie WD. Anaesthetic deaths due to regurgitation or vomiting. Anaesthesia 1951; 6:192. 32. Ruben, A, Ruben, H. Artificial respiration: flow of water from the lung and the stomach. Lancet 1962; 780:81. 33. 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. 34. Lawes, EG, Baskett, PJ. Pulmonary aspiration during unsuccessful cardiopulmonary resuscitation. Intensive Care Med 1987; 13:379. 35. Bjork, RJ, Snyder, BD, Campion, BC, Loewenson, RB. Medical complications of cardiopulmonary arrest. Arch Intern Med 1982; 142:500. 36. Spence, AA, Moir, DD, Finlay, WI. Observations on intragastric pressure. Anaesthesia 1967; 22:249. 37. Weiler, N, Heinrichs, W, Dick, W. Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation. Prehospital Disaster Med 1995; 10:101. 38. Cheifetz, IM, Craig, DM, Quick, G, et al. Increasing tidal volumes and pulmonary overdistention adversely affect pulmonary vascular mechanics and cardiac output in a pediatric swine model. Crit Care Med 1998; 26:710. 39. Berg, MD, Idris, AH, Berg, RA. Severe ventilatory compromise due to gastric distention during pediatric cardiopulmonary resuscitation. Resuscitation 1998; 36:71. 40. Bahr, J, Klingler, H, Panzer, W, et al. Skills of lay people in checking the carotid pulse. Resuscitation 1997; 35:23. 41. Cummins, RO, Hazinski, MF. Cardiopulmonary resuscitation techniques and instruction: when does evidence justify revision? [editorial; comment]. Ann Emerg Med 1999; 34:780. 42. Eberle, B, Dick, WF, Schneider, T, et al. Checking the carotid pulse check: diagnostic accuracy of first responders in patients with and without a pulse. Resuscitation 1996; 33:107. 43. Ochoa, FJ, Ramalle-Gomara, E, Carpintero, JM, et al. Competence of health professionals to check the carotid pulse. Resuscitation 1998; 37:173. 44. Mather, C, O'Kelly, S. The palpation of pulses. Anaesthesia 1996; 51:189. 45. Feneley, MP, Maier, GW, Kern, KB, et al. Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs. Circulation 1988; 77:240. 46. Swenson, RD, Weaver, WD, Niskanen, RA, et al. Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation. Circulation 1988; 78:630. 47. Kern, KB, Sanders, AB, Raife, J, et al. A study of chest compression rates during cardiopulmonary resuscitation in humans. The importance of rate-directed chest compressions. Arch Intern Med 1992; 152:145. 48. Wik, L, Steen, PA. 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Head tilt-chin lift maneuver – If there is no evidence of head or neck trauma, the head tilt-chin lift maneuver is used to open the airway. The rescuer can be beside the victim or behind the victim's head. The palm of one hand is placed on the victim's forehead and firm backward pressure is applied; the fingers (not the thumb) of the other hand are placed on the bony part of the lower jaw near the chin. The lower jaw is moved upward, bringing the chin forward and teeth almost to occlusion; this maneuver supports the jaw and helps tilt the head back. The victim's mouth is opened to facilitate spontaneous breathing and to prepare for mouth-to-mouth breathing. Any dentures should be removed if they cannot be kept in place.
Jaw-thrust maneuver – The jaw-thrust maneuver without tilt is an alternative for opening the airway; it is the safest initial approach to open the airway if neck injury is suspected since it can be performed without extending the neck. With the rescuer behind the victim, one hand is placed on each side of the victim's head, resting the elbows on the surface on which the victim is lying. The angles of the lower jaw are grasped and lifted with both hands. The lower lip can be retracted with the thumb if necessary to open the mouth. If mouth-to-mouth breathing is necessary while maintaining the jaw thrust, the rescuer can close the victim's nostrils by pressing his cheeks tightly against them.
Management of an unconscious victim who is breathing – The victim who is unresponsive, but is breathing and has adequate circulation, should be positioned on his/her side (lateral or modified lateral position) to prevent airway obstruction by the tongue or mucus and to allow adequate drainage of fluid from the mouth. After approximately 30 minutes, the victim should be turned to the opposite side. Several principles should be kept in mind when positioning the victim [24]:
Management of the victim with absent respiration – When respiration is absent, rescue breathing must be provided; this requires adequate inflation of the victim's lungs with each breath.
Complications of rescue breathing – The most common complication of rescue breathing is gastric inflation resulting from excessive ventilation volume and rapid flow rates [28-30]. The risk is also increased because the lower esophageal sphincter relaxes during a cardiac arrest [31]. Marked inflation of the stomach may promote regurgitation, aspiration, and pneumonia [31-35]; the increased intragastric pressure also reduces lung volumes (by elevating the diaphragm) and respiratory system compliance [27,36-39].
Assessment of signs of circulation – The lay person should assess for signs of circulation following the delivery of initial rescue breaths; this includes evaluation for normal breathing, coughing, or movement in response to rescue breathing. The following sequence should be performed:
Chest compressions – Chest compressions for CPR are serial, rhythmic applications of pressure over the lower half of the sternum; these compressions produce blood flow by increasing intrathoracic pressure and directly compressing the heart. A compression rate, ie, the speed of compressions not the actual number delivered in one minute, of 100 per minute is recommended (class IIb) [45-47]. A ratio of 15 compressions to 2 ventilations is recommended for one or two rescuers until the airway is secured [48,49].
Complication of chest compression – Although the risks of chest compression can be minimized by proper hand position, complications can occur even with properly performed chest compression. These include rib fractures, fracture of the sternum, separation of the ribs from the sternum, pneumothorax, hemothorax, lung contusions, laceration of the liver and spleen, and fat embolism.
