European Resuscitation Council Guidelines for Resuscitation ... - CPR

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18 de 0ctubre de 2010 www.elsuapdetodos.com1322 C.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352the oesophagus, air cannot be aspirated because the oesophaguscollapses when aspiration is attempted. The oesophageal detectordevice may be misleading in patients with morbid obesity, latepregnancy or severe asthma or when there are copious trachealsecretions; in these conditions the trachea may collapse when aspirationis attempted. 352,410,415–417 The performance of the syringeoesophageal detector device for identifying tracheal tube positionhas been reported in five cardiac arrest studies 352,418–421 :the sensitivity was 73–100% and the specificity 50–100%. Theperformance of the bulb oesophageal detector device for identifyingtracheal tube position has been reported in three cardiacarrest studies 410,415,421 : the sensitivity was 71–75% and specificity89–100%.Carbon dioxide detectorsCarbon dioxide (CO 2 ) detector devices measure the concentrationof exhaled carbon dioxide from the lungs. The persistence ofexhaled CO 2 after six ventilations indicates placement of the trachealtube in the trachea or a main bronchus. 403 Confirmation ofcorrect placement above the carina will require auscultation of thechest bilaterally in the mid-axillary lines. Broadly, there three typesof carbon dioxide detector device:1. Disposable colorimetric end-tidal carbon dioxide (ETCO 2 ) detectorsuse a litmus paper to detect CO 2 , and these devices generallygive readings of purple (ETCO 2 < 0.5%), tan (ETCO 2 0.5–2%) andyellow (ETCO 2 > 2%). In most studies, tracheal placement of thetube is considered verified if the tan colour persists after afew ventilations. In cardiac arrest patients, eight studies reveal62–100% sensitivity in detecting tracheal placement of the trachealtube and an 86–100% specificity in identifying non-trachealposition. 258,414,420,422–426 Although colorimetric CO 2 detectorsidentify placement in patients with good perfusion quite well,these devices are less accurate than clinical assessment in cardiacarrest patients because pulmonary blood flow may be so lowthat there is insufficient exhaled carbon dioxide. Furthermore, ifthe tracheal tube is in the oesophagus, six ventilations may leadto gastric distension, vomiting and aspiration.2. Non-waveform electronic digital ETCO 2 devices generally measureETCO 2 using an infrared spectrometer and display theresults with a number; they do not provide a waveform graphicaldisplay of the respiratory cycle on a capnograph. Fivestudies of these devices for identification of tracheal tube positionin cardiac arrest document 70–100% sensitivity and 100%specificity. 403,412,414,418,422,4273. End-tidal CO 2 detectors that include a waveform graphical display(capnographs) are the most reliable for verification oftracheal tube position during cardiac arrest. Two studies ofwaveform capnography to verify tracheal tube position in victimsof cardiac arrest demonstrate 100% sensitivity and 100%specificity in identifying correct tracheal tube placement. 403,428Three studies with a cumulative total of 194 tracheal and 22oesophageal tube placements documented an overall 64% sensitivityand 100% specificity in identifying correct tracheal tubeplacement when using a capnograph in prehospital cardiacarrest victims. 410,415,421 However, in these studies intubationwas undertaken only after arrival at hospital (time to intubationaveraged more than 30 min) and many of the cardiac arrestvictims studied had prolonged resuscitation times and very prolongedtransport time.Based on the available data, the accuracy of colorimetric CO 2detectors, oesophageal detector devices and non-waveform capnometersdoes not exceed the accuracy of auscultation and directvisualization for confirming the tracheal position of a tube in victimsof cardiac arrest. Waveform capnography is the most sensitiveand specific way to confirm and continuously monitor the positionof a tracheal tube in victims of cardiac arrest and should supplementclinical assessment (auscultation and visualization of tube throughcords). Waveform capnography will not discriminate between trachealand bronchial placement of the tube—careful auscultationis essential. Existing portable monitors make capnographic initialconfirmation and continuous monitoring of tracheal tube positionfeasible in almost all settings, including out-of-hospital, emergencydepartment, and in-hospital locations where intubation isperformed. In the absence of a waveform capnograph it may bepreferable to use a supraglottic airway device when advanced airwaymanagement is indicated.Thoracic impedanceThere are smaller changes in thoracic impedance withoesophageal ventilations than with ventilation of the lungs. 429–431Changes in thoracic impedance may be used to detect ventilation 432and oesphageal intubation 402,433 during cardiac arrest. It is possiblethat this technology can be used to measure tidal volume duringCPR. The role of thoracic impedance as a tool to detect tracheal tubeposition and adequate ventilation during CPR is undergoing furtherresearch but is not yet ready for routine clinical use.Cricoid pressureIn non-arrest patients cricoid pressure may offer some measureof protection to the airway from aspiration but it may also impedeventilation or interfere with intubation. The role of cricoid duringcardiac arrest has not been studied. Application of cricoid pressureduring bag-mask ventilation reduces gastric inflation. 334,335,434,435Studies in anaesthetised patients show that cricoid pressureimpairs ventilation in many patients, increases peak inspiratorypressures and causes complete obstruction in up to 50% of patientsdepending on the amount of cricoid pressure (in the range of recommendedeffective pressure) that is applied. 334–339,436,437The routine use of cricoid pressure in cardiac arrest is not recommended.If cricoid pressure is used during cardiac arrest, thepressure should be adjusted, relaxed or released if it impedes ventilationor intubation.Securing the tracheal tubeAccidental dislodgement of a tracheal tube can occur at any time,but may be more likely during resuscitation and during transport.The most effective method for securing the tracheal tube has yet tobe determined; use either conventional tapes or ties, or purposemadetracheal tube holders.www.elsuapdetodos.comCricothyroidotomyOccasionally it will be impossible to ventilate an apnoeic patientwith a bag-mask, or to pass a tracheal tube or alternative airwaydevice. This may occur in patients with extensive facial traumaor laryngeal obstruction caused by oedema or foreign material.In these circumstances, delivery of oxygen through a needle orsurgical cricothyroidotomy may be life-saving. A tracheostomy iscontraindicated in an emergency, as it is time consuming, hazardousand requires considerable surgical skill and equipment.Surgical cricothyroidotomy provides a definitive airway that canbe used to ventilate the patient’s lungs until semi-elective intubationor tracheostomy is performed. Needle cricothyroidotomyis a much more temporary procedure providing only short-termoxygenation. It requires a wide-bore, non-kinking cannula, a highpressureoxygen source, runs the risk of barotrauma and can beparticularly ineffective in patients with chest trauma. It is also
prone to failure because of kinking of the cannula, and is unsuitablefor patient transfer.4f Assisting the circulationDrugs and fluids for cardiac arrestThis topic is divided into: drugs used during the managementof a cardiac arrest; anti-arrhythmic drugs used in the peri-arrestperiod; other drugs used in the peri-arrest period; fluids; and routesfor drug delivery. Every effort has been made to provide accurateinformation on the drugs in these guidelines, but literature fromthe relevant pharmaceutical companies will provide the most upto-datedata.Drugs used during the treatment of cardiac arrestOnly a few drugs are indicated during the immediate managementof a cardiac arrest, and there is limited scientific evidencesupporting their use. Drugs should be considered only after initialshocks have been delivered (if indicated) and chest compressionsand ventilation have been started. The evidence for the optimaltiming and order of drug delivery, and the optimal dose, is limited.There are three groups of drugs relevant to the management ofcardiac arrest that were reviewed during the 2010 Consensus Conference:vasopressors, anti-arrhythmics and other drugs. Routes ofdrug delivery other than the optimal intravenous route were alsoreviewed and are discussed.VasopressorsDespite the continued widespread use of adrenaline andincreased use of vasopressin during resuscitation in some countries,there is no placebo-controlled study that shows that theroutine use of any vasopressor during human cardiac arrestincreases survival to hospital discharge, although improved shorttermsurvival has been documented. 245,246 The primary goal ofcardiopulmonary resuscitation is to re-establish blood flow to vitalorgans until the restoration of spontaneous circulation. Despite thelack of data from cardiac arrest in humans, vasopressors continueto be recommended as a means of increasing cerebral and coronaryperfusion during CPR.Adrenaline (epinephrine) versus vasopressinAdrenaline has been the primary sympathomimetic agentfor the management of cardiac arrest for 40 years. 438 Itsalpha-adrenergic, vasoconstrictive effects cause systemic vasoconstriction,which increases coronary and cerebral perfusionpressures. The beta-adrenergic actions of adrenaline (inotropic,chronotropic) may increase coronary and cerebral blood flow, butconcomitant increases in myocardial oxygen consumption, ectopicventricular arrhythmias (particularly when the myocardium isacidotic), transient hypoxaemia due to pulmonary arteriovenousshunting, impaired microcirculation, 281 and worse post-cardiacarrest myocardial dysfunction 283,284 may offset these benefits.The potentially deleterious beta-effects of adrenaline have ledto exploration of alternative vasopressors. Vasopressin is a naturallyoccurring antidiuretic hormone. In very high doses it is apowerful vasoconstrictor that acts by stimulation of smooth muscleV1 receptors. Three randomised controlled trials 439–441 and ameta-analysis 442 demonstrated no difference in outcomes (ROSC,survival to discharge, or neurological outcome) with vasopressinversus adrenaline as a first line vasopressor in cardiac arrest. Twomore recent studies comparing adrenaline alone or in combinationwith vasopressin also demonstrated no difference in ROSC, survival18 de 0ctubre de 2010 www.elsuapdetodos.comC.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352 1323to discharge or neurological outcome. 443,444 There are no alternativevasopressors that provide survival benefit during cardiac arrestresuscitation when compared with adrenaline.Participants at the 2010 Consensus Conference debated in depththe treatment recommendations that should follow from this evidence.Despite the absence of data demonstrating an increase inlong-term survival, adrenaline has been the standard vasopressorin cardiac arrest. It was agreed that there is currently insufficientevidence to support or refute the use of any other vasopressor asan alternative to, or in combination with, adrenaline in any cardiacarrest rhythm to improve survival or neurological outcome. Currentpractice still supports adrenaline as the primary vasopressor for thetreatment of cardiac arrest of all rhythms. Although the evidenceof benefit from the use of adrenaline is limited, it was felt that theimproved short-term survival documented in some studies 245,246warranted its continued use, although in the absence of clinicalevidence, the dose and timing have not been changed in the 2010guidelines.AdrenalineIndications.• Adrenaline is the first drug used in cardiac arrest of any cause:it is included in the ALS algorithm for use every 3–5 min of CPR(alternate cycles).• Adrenaline is preferred in the treatment of anaphylaxis (Section8g). 294• Adrenaline is a second-line treatment for cardiogenic shock.Dose. During cardiac arrest, the initial IV/IO dose of adrenalineis 1 mg. There are no studies showing survival benefit for higherdoses of adrenaline for patients in refractory cardiac arrest. In somecases, an adrenaline infusion is required in the post-resuscitationperiod.Following return of spontaneous circulation, even small dosesof adrenaline (50–100 g) may induce tachycardia, myocardialischaemia, VT and VF. Once a perfusing rhythm is established, iffurther adrenaline is deemed necessary, titrate the dose carefully toachieve an appropriate blood pressure. Intravenous doses of 50 gare usually sufficient for most hypotensive patients. Use adrenalinecautiously in patients with cardiac arrest associated with cocaineor other sympathomimetic drugs.Use.www.elsuapdetodos.comAdrenaline is available most commonly in two dilutions:• 1 in 10,000 (10 ml of this solution contains 1 mg of adrenaline).• 1 in 1000 (1 ml of this solution contains 1 mg of adrenaline).Both these dilutions are used routinely in Europe.Anti-arrhythmicsAs with vasopressors, the evidence that anti-arrhythmic drugsare of benefit in cardiac arrest is limited. No anti-arrhythmic druggiven during human cardiac arrest has been shown to increase survivalto hospital discharge, although amiodarone has been shownto increase survival to hospital admission. 285,286 Despite the lackof human long-term outcome data, the balance of evidence is infavour of the use anti-arrhythmic drugs for the management ofarrhythmias in cardiac arrest.AmiodaroneAmiodarone is a membrane-stabilising anti-arrhythmic drugthat increases the duration of the action potential and refractoryperiod in atrial and ventricular myocardium. Atrioventricular
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European Resuscitation Council Guidelines for Resuscitation ... - CPR

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