European Resuscitation Council Guidelines for Resuscitation ... - CPR

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18 de 0ctubre de 2010 www.elsuapdetodos.com1412 J. Soar et al. / Resuscitation 81 (2010) 1400–1433and advanced life support and cool the patient. Cooling techniquessimilar to those used to induce therapeutic hypothermia shouldbe used (see Section 4g). 24a There are no data on the effects ofhyperthermia on defibrillation threshold; therefore, attempt defibrillationaccording to current guidelines, while continuing to coolthe patient. Animal studies suggest the prognosis is poor comparedwith normothermic cardiac arrest. 293,294 The risk of unfavourableneurological outcome increases for each degree of body temperature>37 ◦ C. 295 Provide post-resuscitation care according to normalguidelines.8f. AsthmaIntroductionWorldwide, approximately 300 million people of all ages andethnic backgrounds have asthma. 296 The worldwide prevalence ofasthma symptoms ranges from 1 to 18% of the population witha high prevalence in some European countries (United Kingdom,Ireland and Scandinavia). 296 International differences in asthmasymptom prevalence appears to be decreasing in recent years,especially in adolescents. 297 The World Health Organisation hasestimated that 15 million disability-adjusted life-years (DALYs) arelost annually from asthma, representing 1% of the global diseaseburden. Annual worldwide deaths from asthma have been estimatedat 250,000. The death rate does not appear to be correlatedwith asthma prevalence. 296 National and international guidancefor the management of asthma already exists. 296,298 This guidancefocuses on the treatment of patients with near-fatal asthma andcardiac arrest.Patients at risk of asthma-related cardiac arrestThe risk of near-fatal asthma attacks is not necessarily relatedto asthma severity. 299 Patients most at risk include those with:• a history of near-fatal asthma requiring intubation and mechanicalventilation;• a hospitalisation or emergency care for asthma in the pastyear 300 ;• low or no use of inhaled corticosteroids 301 ;• an increasing use and dependence of beta-2 agonists 302 ;• anxiety, depressive disorders and/or poor compliance withtherapy. 303Causes of cardiac arrestCardiac arrest in a person with asthma is often a terminal eventafter a period of hypoxaemia; occasionally, it may be sudden. Cardiacarrest in those with asthma has been linked to:• severe bronchospasm and mucous plugging leading to asphyxia(this condition causes the vast majority of asthma-relateddeaths);• cardiac arrhythmias caused by hypoxia, which is the commonestcause of asthma-related arrhythmia. 304 Arrhythmias can also becaused by stimulant drugs (e.g., beta-adrenergic agonists, aminophylline)or electrolyte abnormalities;• dynamic hyperinflation, i.e., auto-positive end-expiratory pressure(auto-PEEP), can occur in mechanically ventilated asthmatics.Auto-PEEP is caused by air trapping and ‘breath stacking’ (airentering the lungs and being unable to escape). Gradual build-upof pressure occurs and reduces venous return and blood pressure;• tension pneumothorax (often bilateral).DiagnosisWheezing is a common physical finding, but severity doesnot correlate with the degree of airway obstruction. The absenceof wheezing may indicate critical airway obstruction, whereasincreased wheezing may indicate a positive response to bronchodilatortherapy. SaO 2 may not reflect progressive alveolarhypoventilation, particularly if oxygen is being given. The SaO 2may initially decrease during therapy because beta-agonists causeboth bronchodilation and vasodilation and may initially increaseintrapulmonary shunting.Other causes of wheezing include: pulmonary oedema,chronic obstructive pulmonary disease (COPD), pneumonia,anaphylaxis, 305 pneumonia, foreign bodies, pulmonary embolism,bronchiectasis and subglottic mass. 306The severity of an asthma attack is defined in Table 8.3.Key interventions to prevent arrestThe patient with severe asthma requires aggressive medicalmanagement to prevent deterioration. Base assessment and treatmenton an ABCDE approach. Patients with SaO 2 < 92% or withfeatures of life-threatening asthma are at risk of hypercapnia andrequire arterial blood gas measurement. Experienced cliniciansshould treat these high-risk patients in a critical-care area. The specificdrugs and the treatment sequence will vary according to localpractice.OxygenUse a concentration of inspired oxygen that will achieve an SaO 294–98%. 205 High-flow oxygen by mask is sometimes necessary.Table 8.3The severity of asthma.AsthmaNear-fatalLife-threateningwww.elsuapdetodos.comAcute severeModerateexacerbationFeaturesRaised PaCO 2 and/or requiringmechanical ventilation with raisedinflation pressuresAny one of:PEF < 33% best or predictedbradycardiaSpO 2 < 92%, dysrhythmiaPaO 2 < 8 kPa, hypotensionNormal PaCO 2 (4.6–6.0 kPa(35–45 mmHg)), exhaustionSilent chest, confusionCyanosis, comaFeeble respiratory effortAny one of:PEF 33–50% best or predictedRespiratory rate > 25 min −1Heart rate > 110 min −1Inability to complete sentences inone breathIncreasing symptomsPEF > 50–75% best or predictedNo features of acute severe asthmaBrittle Type 1: wide PEF variability (>40%diurnal variation for >50% of thetime over a period >150 days)despite intense therapyType 2: sudden severe attacks on abackground of apparently wellcontrolled asthmaPEF, peak expiratory flow.
18 de 0ctubre de 2010 www.elsuapdetodos.comJ. Soar et al. / Resuscitation 81 (2010) 1400–1433 1413Nebulised beta-2 agonistsSalbutamol, 5 mg nebulised, is the cornerstone of therapyfor acute asthma in most of the world. Repeated doses every15–20 min are often needed. Severe asthma may necessitate continuousnebulised salbutamol. Nebuliser units that can be drivenby high-flow oxygen should be available. The hypoventilationassociated with severe or near-fatal asthma may prevent effectivedelivery of nebulised drugs. If a nebuliser is not immediatelyavailable beta-2 agonists can be temporarily administered byrepeating activations of a metered dose inhaler via a large volumespacer device. 298,307 Nebulised adrenaline does not provide additionalbenefit over and above nebulised beta-2 agonists in acuteasthma. 308Intravenous corticosteroidsto report in 2012 and should provide definitive evidence on the roleof magnesium in acute severe asthma.AminophyllineA Cochrane review of intravenous aminophylline found noevidence of benefit and a higher incidence of adverse effects(tachycardia, vomiting) compared with standard care alone. 316,317Whether aminophylline has a place as an additional therapy aftertreatment with established medications such as inhaled betaagonistsand systemic corticosteroids remains uncertain. If afterobtaining senior advice the decision is taken to administer IVaminophylline a loading dose of 5 mg kg −1 is given over 20–30 min(unless on maintenance therapy), followed by an infusion of500–700 gkg −1 h −1 . Serum theophylline concentrations shouldbe maintained below 20 gml −1 to avoid toxicity.Early use of systemic corticosteroids for acute asthma in theemergency department significantly reduces hospital admissionrates, especially for those patients not receiving concomitant corticosteroidtherapy. 309 Although there is no difference in clinicaleffects between oral and IV formulations of corticosteroids, 310 theIV route is preferable because patients with near-fatal asthma mayvomit or be unable to swallow.Nebulised anticholinergicsNebulised anticholinergics (ipratropium, 0.5 mg 4–6 hourly)may produce additional bronchodilation in severe asthma or inthose who do not respond to beta-agonists. 311,312Nebulised magnesium sulphateResults of small randomised controlled trials showed that a nebulisedisotonic solution of magnesium sulphate (250 mmol l −1 )inavolume of 2.5–5 ml in combination with beta-2 agonists is safe andit is associated with both an improvement of pulmonary functiontests and a non-significant trend towards lower rates of hospitaladmission in patients with acute severe asthma. 313 Further studiesare needed to confirm those findings.Intravenous bronchodilatorsNebulised bronchodilators are the first line treatment for acutesevere and life-threatening exacerbations of asthma. There is alack of definitive evidence for or against the use of intravenousbronchodilators in this setting. Trials have primarily included spontaneouslybreathing patients with moderate to life-threateningexacerbations of asthma, evidence in ventilated patients withlife-threatening asthma or cardiac arrest is sparse. The use of intravenousbronchodilators should generally be restricted to patientsunresponsive to nebulised therapy or where nebulised/inhaledtherapy is not possible (e.g., a patient receiving bag-mask ventilation).Intravenous magnesium sulphateStudies of intravenous magnesium sulphate in acute severe andlife-threatening asthma have produced conflicting results. 314,315Magnesium sulphate causes bronchial smooth muscle relaxationindependent of the serum magnesium level and has only minor sideeffects (flushing, light-headedness). Given the low risk of seriousside effects from magnesium sulphate it would seem reasonable touse intravenous magnesium sulphate (1.2–2 g IV slowly) in adultswith life-threatening unresponsive to nebulised therapy. The multicentrerandomised controlled trial 3Mg (ISRCTN04417063) is dueBeta-2 agonistsA Cochrane review on intravenous beta-2 agonists comparedwith nebulised beta-2 agonists found no evidence of benefit andsome evidence of increased side effects compared with inhaledtreatment. 318 Salbutamol may be given as either a slow IV injection(250 g IV slowly) or continuous infusion of 3–20 g min −1 .Leukotriene receptor antagonistsThere are few data on the use of intravenous leukotriene receptorantagonists. 319 Further studies are required to confirm thefindings of a recent randomised controlled trial which demonstratedevidence of additional bronchodilation when intravenousLRTA montelukast was used as a rescue therapy. 320Subcutaneous or intramuscular adrenaline and terbutalineAdrenaline and terbutaline are adrenergic agents that may begiven subcutaneously to patients with acute severe asthma. Thedose of subcutaneous adrenaline is 300 g up to a total of 3 dosesat 20-min intervals. Adrenaline may cause an increase in heart rate,myocardial irritability and increased oxygen demand; however,its use (even in patients over 35-years old) is well tolerated. 321Terbutaline is given in a dose of 250 g subcutaneously, which canbe repeated in 30–60 min. These drugs are more commonly givento children with acute asthma and, although most studies haveshown them to be equally effective, 322 one study concluded thatterbutaline was superior. 323 These alternative routes may need tobe considered when IV access is impossible. Patients with asthmaare at increased risk of anaphylaxis. Sometimes it may be difficultto distinguish severe life-threatening asthma from anaphylaxis. Inthese circumstances intramuscular adrenaline given according tothe anaphylaxis guidelines may be appropriate (Section 8g).www.elsuapdetodos.comIntravenous fluids and electrolytesSevere or near-fatal asthma is associated with dehydration andhypovolaemia, and this will further compromise the circulationin patients with dynamic hyperinflation of the lungs. If there isevidence of hypovolaemia or dehydration, give IV fluids. Beta-2agonists and steroids may induce hypokalaemia, which should becorrected with electrolyte supplements.HelioxHeliox is a mixture of helium and oxygen (usually 80:20 or70:30). A meta-analysis of four clinical trials did not support the useof heliox in the initial treatment of patients with acute asthma. 324
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