European Resuscitation Council Guidelines for Resuscitation ... - CPR

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18 de 0ctubre de 2010 www.elsuapdetodos.com1238 J.P. Nolan et al. / Resuscitation 81 (2010) 1219–1276TachycardiasIf the patient is unstableIf the patient is unstable and deteriorating, with any of theadverse signs and symptoms described above being caused bythe tachycardia, attempt synchronised cardioversion immediately(Fig. 1.7). In patients with otherwise normal hearts, serioussigns and symptoms are uncommon if the ventricular rate is
to pharmacological treatments or with risks factors for asystole(Fig. 1.8).Post-resuscitation careSuccessful ROSC is the just the first step toward the goalof complete recovery from cardiac arrest. The post-cardiacarrest syndrome, which comprises post-cardiac arrest braininjury, post-cardiac arrest myocardial dysfunction, the systemicischaemia/reperfusion response, and the persistent precipitatingpathology, often complicates the post-resuscitation phase. 3The severity of this syndrome will vary with the duration andcause of cardiac arrest. It may not occur at all if the cardiacarrest is brief. Post-cardiac arrest brain injury manifestsas coma, seizures, myoclonus, varying degrees of neurocognitivedysfunction and brain death. Among patients surviving toICU admission but subsequently dying in-hospital, brain injuryis the cause of death in 68% after out-of-hospital cardiac arrestand in 23% after in-hospital cardiac arrest. 227,305 Post-cardiacarrest brain injury may be exacerbated by microcirculatory failure,impaired autoregulation, hypercarbia, hyperoxia, pyrexia,hyperglycaemia and seizures. Significant myocardial dysfunctionis common after cardiac arrest but typically recovers by 2–3days. 306,307 The whole body ischaemia/reperfusion of cardiac arrestactivates immunological and coagulation pathways contributing tomultiple organ failure and increasing the risk of infection. 308,309Thus, the post-cardiac arrest syndrome has many features in commonwith sepsis, including intravascular volume depletion andvasodilation. 310,311Airway and breathingHypoxaemia and hypercarbia both increase the likelihood of afurther cardiac arrest and may contribute to secondary brain injury.Several animal studies indicate that hyperoxaemia causes oxidativestress and harms post-ischaemic neurones. 273,312–315 A clinicalregistry study documented that post-resuscitation hyperoxaemiawas associated with worse outcome, compared with both normoxaemiaand hypoxaemia. 274 In clinical practice, as soon as arterialblood oxygen saturation can be monitored reliably (by blood gasanalysis and/or pulse oximetry), it may be more practicable totitrate the inspired oxygen concentration to maintain the arterialblood oxygen saturation in the range of 94–98%. Consider trachealintubation, sedation and controlled ventilation in any patient withobtunded cerebral function. There are no data to support the targetingof a specific arterial PCO 2 after resuscitation from cardiac arrest,but it is reasonable to adjust ventilation to achieve normocarbiaand to monitor this using the end-tidal PCO 2 and arterial blood gasvalues.Circulation18 de 0ctubre de 2010 www.elsuapdetodos.comJ.P. Nolan et al. / Resuscitation 81 (2010) 1219–1276 1239definitive data, target the mean arterial blood pressure to achievean adequate urine output (1 ml kg −1 h −1 ) and normal or decreasingplasma lactate values, taking into consideration the patient’s normalblood pressure, the cause of the arrest and the severity of anymyocardial dysfunction. 3Disability (optimizing neurological recovery)Control of seizuresSeizures or myoclonus or both occur in 5–15% of adultpatients who achieve ROSC and 10–40% of those who remaincomatose. 58,327–330 Seizures increase cerebral metabolism by upto 3-fold 331 and may cause cerebral injury: treat promptly andeffectively with benzodiazepines, phenytoin, sodium valproate,propofol, or a barbiturate. No studies directly address the use ofprophylactic anticonvulsant drugs after cardiac arrest in adults.Glucose controlThere is a strong association between high blood glucoseafter resuscitation from cardiac arrest and poor neurologicaloutcome. 58,332–338 A large randomised trial of intensive glucosecontrol (4.5–6.0 mmol l −1 ) versus conventional glucose control(10 mmol l −1 or less) in general ICU patients reported increased 90-day mortality in patients treated with intensive glucose control. 339Another recent study and two meta-analyses of studies of tightglucose control versus conventional glucose control in critically illpatients showed no significant difference in mortality but foundtight glucose control was associated with a significantly increasedrisk of hypoglycaemia. 340–342 Severe hypoglycaemia is associatedwith increased mortality in critically ill patients, 343 and comatosepatients are at particular risk from unrecognised hypoglycaemia.There is some evidence that, irrespective of the target range, variabilityin glucose values is associated with mortality. 344 Based onthe available data, following ROSC blood glucose should be maintainedat ≤10 mmol l −1 (180 mg dl −1 ). 345 Hypoglycaemia should beavoided. Strict glucose control should not be implemented in adultpatients with ROSC after cardiac arrest because of the increased riskof hypoglycaemia.Temperature controlTreatment of hyperpyrexia. A period of hyperthermia (hyperpyrexia)is common in the first 48 h after cardiac arrest. 346–348Several studies document an association between post-cardiacarrest pyrexia and poor outcomes. 58,346,348–351 There are no randomisedcontrolled trials evaluating the effect of treatment ofpyrexia (defined as ≥37.6 ◦ C) compared to no temperature controlin patients after cardiac arrest. Although the effect of elevatedtemperature on outcome is not proved, it seems prudent to treatany hyperthermia occurring after cardiac arrest with antipyreticsor active cooling.www.elsuapdetodos.comIt is well recognised that post-cardiac arrest patients withSTEMI should undergo early coronary angiography and percutaneouscoronary intervention (PCI) but, because chest pain and/orST elevation are poor predictors of acute coronary occlusion inthese patients, 316 this intervention should be considered in allpost-cardiac arrest patients who are suspected of having coronaryartery disease. 316–324 Several studies indicate that the combinationof therapeutic hypothermia and PCI is feasible and safe after cardiacarrest caused by acute myocardial infarction. 317,323–326Post-cardiac arrest myocardial dysfunction causes haemodynamicinstability, which manifests as hypotension, low cardiacindex and arrhythmias. 306 If treatment with fluid resuscitation andvasoactive drugs is insufficient to support the circulation, considerinsertion of an intra-aortic balloon pump. 317,325 In the absence ofTherapeutic hypothermia. Animal and human data indicatethat mild hypothermia is neuroprotective and improves outcomeafter a period of global cerebral hypoxia-ischaemia. 352,353 Coolingsuppresses many of the pathways leading to delayed celldeath, including apoptosis (programmed cell death). Hypothermiadecreases the cerebral metabolic rate for oxygen (CMRO 2 )byabout 6% for each 1 ◦ C reduction in temperature 354 and this mayreduce the release of excitatory amino acids and free radicals. 352Hypothermia blocks the intracellular consequences of excitotoxinexposure (high calcium and glutamate concentrations) and reducesthe inflammatory response associated with the post-cardiac arrestsyndrome.All studies of post-cardiac arrest therapeutic hypothermia haveincluded only patients in coma. There is good evidence supporting
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European Resuscitation Council Guidelines for Resuscitation ... - CPR

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