European Resuscitation Council Guidelines for Resuscitation ... - CPR

18 de 0ctubre de 2010 www.elsuapdetodos.com1334 C.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352discharge, the vast majority have a good neurological outcomealthough many with some cognitive impairment. 639Post-cardiac arrest syndromeObtain a chest radiograph to check the position of the tracheal tubeand central venous lines, assess for pulmonary oedema, and detectcomplications from CPR such as a pneumothorax associated withrib fractures.The post-cardiac arrest syndrome comprises post-cardiac arrestbrain injury, post-cardiac arrest myocardial dysfunction, thesystemic ischaemia/reperfusion response, and the persistent precipitatingpathology. 628 The severity of this syndrome will varywith the duration and cause of cardiac arrest. It may not occurat all if the cardiac arrest is brief. Post-cardiac arrest brain injurymanifests as coma, seizures, myoclonus, varying degrees of neurocognitivedysfunction and brain death. Among patients survivingto ICU admission but subsequently dying in-hospital, brain injury isthe cause of death in 68% after out-of hospital cardiac arrest and in23% after in-hospital cardiac arrest. 245,640 Post-cardiac arrest braininjury may be exacerbated by microcirculatory failure, impairedautoregulation, hypercarbia, hyperoxia, pyrexia, hyperglycaemiaand seizures. Significant myocardial dysfunction is common aftercardiac arrest but typically recovers by 2–3 days. 641,642 The wholebody ischaemia/reperfusion of cardiac arrest activates immunologicaland coagulation pathways contributing to multiple organfailure and increasing the risk of infection. 643,644 Thus, the postcardiacarrest syndrome has many features in common with sepsis,including intravascular volume depletion and vasodilation. 645,646Airway and breathingPatients who have had a brief period of cardiac arrest respondingimmediately to appropriate treatment may achieve an immediatereturn of normal cerebral function. These patients do not requiretracheal intubation and ventilation but should be given oxygen viaa facemask. Hypoxaemia and hypercarbia both increase the likelihoodof a further cardiac arrest and may contribute to secondarybrain injury. Several animal studies indicate that hyperoxaemiacauses oxidative stress and harms post-ischaemic neurones. 647–650One animal study has demonstrated that adjusting the fractionalinspired concentration (FiO 2 ) to produce an arterial oxygensaturation of 94–96% in the first hour after ROSC (‘controlled reoxygenation’)achieved better neurological outcomes than achievedwith the delivery of 100% oxygen. 328 A recent clinical registry studythat included more than 6000 patients supports the animal data andshows post-resuscitation hyperoxaemia is associated with worseoutcome, compared with both normoxaemia and hypoxaemia. 329In clinical practice, as soon as arterial blood oxygen saturation canbe monitored reliably (by blood gas analysis and/or pulse oximetry),it may be more practicable to titrate the inspired oxygenconcentration to maintain the arterial blood oxygen saturation inthe range of 94–98%.Consider tracheal intubation, sedation and controlled ventilationin any patient with obtunded cerebral function. Ensurethe tracheal tube is positioned correctly well above the carina.Hypocarbia causes cerebral vasoconstriction and a decreased cerebralblood flow. 651 After cardiac arrest, hypocapnoea induced byhyperventilation causes cerebral ischaemia. 652–655 There are nodata to support the targeting of a specific arterial PCO 2 after resuscitationfrom cardiac arrest, but it is reasonable to adjust ventilationto achieve normocarbia and to monitor this using the end-tidalPCO 2 and arterial blood gas values.Insert a gastric tube to decompress the stomach; gastric distensioncaused by mouth-to-mouth or bag-mask-valve ventilation willsplint the diaphragm and impair ventilation. Give adequate doses ofsedative, which will reduce oxygen consumption. Bolus doses of aneuromuscular blocking drug may be required, particularly if usingtherapeutic hypothermia (see below), but try to avoid infusions ofneuromuscular blocking drugs because these may mask seizures.CirculationThe majority of out-of-hospital cardiac arrest patients havecoronary artery disease. 656,657 Acute changes in coronary plaquemorphology occur in 40–86% of cardiac arrest survivors and in15–64% of autopsy studies. 658 It is well recognised that postcardiacarrest patients with ST elevation myocardial infarction(STEMI) should undergo early coronary angiography and percutaneouscoronary intervention (PCI) but, because chest painand/or ST elevation are poor predictors of acute coronary occlusionin these patients, 659 this intervention should be consideredin all post-cardiac arrest patients who are suspected of havingcoronary artery disease. 629,633,659–665 Several studies indicatethat the combination of therapeutic hypothermia and PCI is feasibleand safe after cardiac arrest caused by acute myocardialinfarction. 629,633,638,665,666Post-cardiac arrest myocardial dysfunction causes haemodynamicinstability, which manifests as hypotension, low cardiacindex and arrhythmias. 641 Early echocardiography will enable thedegree of myocardial dysfunction to be quantified. 642 In the ICUan arterial line for continuous blood pressure monitoring is essential.Treatment with fluid, inotropes and vasopressors may beguided by blood pressure, heart rate, urine output, and rate ofplasma lactate clearance and central venous oxygen saturations.Non-invasive cardiac output monitors may help to guide treatmentbut there is no evidence that their use affects outcome. Iftreatment with fluid resuscitation and vasoactive drugs is insufficientto support the circulation, consider insertion of an intra-aorticballoon pump. 629,638 Infusion of relatively large volumes of fluidsare tolerated remarkably well by patients with post-cardiacarrest syndrome. 513,629,630,641 Although early goal directed therapyis well-established in the treatment of sepsis, 667 and hasbeen proposed as a treatment strategy after cardiac arrest, 630there are no randomised, controlled data to support its routineuse.There are very few randomised trials evaluating the role ofblood pressure on the outcome after cardiac arrest. One randomisedstudy demonstrated no difference in the neurological outcomeamong patients randomised to a mean arterial blood pressure(MAP) of >100 mm Hg versus ≤100 mm Hg 5 min after ROSC; however,good functional recovery was associated with a higher bloodpressure during the first 2 h after ROSC. 668 In a registry study ofmore than 6000 post-cardiac arrest patients, hypotension (systolicblood pressure