European Resuscitation Council Guidelines for Resuscitation ... - CPR

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18 de 0ctubre de 2010 www.elsuapdetodos.com1324 C.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352conduction is slowed, and a similar effect is seen with accessorypathways. Amiodarone has a mild negative inotropic action andcauses peripheral vasodilation through non-competitive alphablockingeffects. The hypotension that occurs with intravenousamiodarone is related to the rate of delivery and is due moreto the solvent (Polysorbate 80 and benzyl alcohol), which causeshistamine release, rather than the drug itself. 445 The use of anaqueous amiodarone preparation that is relatively free from theseside effects has recently been approved for use in the UnitedStates. 446,447Following three initial shocks, amiodarone in shock-refractoryVF improves the short-term outcome of survival to hospital admissioncompared with placebo 285 or lidocaine. 286 Amiodarone alsoappears to improve the response to defibrillation when given tohumans or animals with VF or haemodynamically unstable ventriculartachycardia. 446–450 There is no evidence to indicate the optimaltime at which amiodarone should be given when using a singleshockstrategy. In the clinical studies to date, the amiodarone wasgiven if VF/VT persisted after at least three shocks. For this reason,and in the absence of any other data, amiodarone 300 mg isrecommended if VF/VT persists after three shocks.Indications.Amiodarone is indicated in• refractory VF/VT;• haemodynamically stable ventricular tachycardia (VT) and otherresistant tachyarrhythmias (Section 4g).Dose. Consider an initial intravenous dose of 300 mg amiodarone,diluted in 5% dextrose (or other suitable solvent) to avolume of 20 ml (or from a pre-filled syringe), if VF/VT persistsafter the third shock. Give a further dose of 150 mg if VF/VT persists.Amiodarone can cause thrombophlebitis when injected intoa peripheral vein; use a central vein if a central venous catheter is insitu but, if not, use a large peripheral vein or the IO route followedby a generous flush. Details about the use of amiodarone for thetreatment of other arrhythmias are given in Section 4g.Clinical aspects of use. Amiodarone may paradoxically bearrhythmogenic, especially if given concurrently with drugs thatprolong the QT interval. However, it has a lower incidence ofpro-arrhythmic effects than other anti-arrhythmic drugs undersimilar circumstances. The major acute adverse effects from amiodaroneare hypotension and bradycardia, which can be preventedby slowing the rate of drug infusion, or can be treated with fluidsand/or inotropic drugs. The side effects associated with prolongedoral use (abnormalities of thyroid function, corneal microdeposits,peripheral neuropathy, and pulmonary/hepatic infiltrates) are notrelevant in the acute setting.LidocaineUntil the publication of the 2000 ILCOR guidelines, lidocainewas the anti-arrhythmic drug of choice. Comparative studies withamiodarone 286 have displaced it from this position, and lidocaineis now recommended only when amiodarone is unavailable.Amiodarone should be available at all hospital arrests and at allout-of-hospital arrests attended by emergency medical services.Lidocaine is a membrane-stabilising anti-arrhythmic drug thatacts by increasing the myocyte refractory period. It decreases ventricularautomaticity, and its local anaesthetic action suppressesventricular ectopic activity. Lidocaine suppresses activity of depolarised,arrhythmogenic tissues while interfering minimally withthe electrical activity of normal tissues. Therefore, it is effectivein suppressing arrhythmias associated with depolarisation (e.g.,ischaemia, digitalis toxicity) but is relatively ineffective againstarrhythmias occurring in normally polarised cells (e.g., atrial fibrillation/flutter).Lidocaine raises the threshold for VF.Lidocaine toxicity causes paraesthesia, drowsiness, confusionand muscular twitching progressing to convulsions. It is consideredgenerally that a safe dose of lidocaine must not exceed 3 mg kg −1over the first hour. If there are signs of toxicity, stop the infusionimmediately; treat seizures if they occur. Lidocaine depressesmyocardial function, but to a much lesser extent than amiodarone.The myocardial depression is usually transient and can be treatedwith intravenous fluids or vasopressors.Indications. Lidocaine is indicated in refractory VF/VT (whenamiodarone is unavailable).Dose. When amiodarone is unavailable, consider an initial doseof 100 mg (1–1.5 mg kg −1 ) of lidocaine for VF/pulseless VT refractoryto three shocks. Give an additional bolus of 50 mg if necessary.The total dose should not exceed 3 mg kg −1 during the first hour.Clinical aspects of use. Lidocaine is metabolised by the liver, andits half-life is prolonged if the hepatic blood flow is reduced, e.g.,in the presence of reduced cardiac output, liver disease or in theelderly. During cardiac arrest normal clearance mechanisms do notfunction, thus high plasma concentrations may be achieved after asingle dose. After 24 h of continuous infusion, the plasma half-lifeincreases significantly. Reduce the dose in these circumstances, andregularly review the indication for continued therapy. Lidocaine isless effective in the presence of hypokalaemia and hypomagnesaemia,which should be corrected immediately.MagnesiumMagnesium is an important constituent of many enzyme systems,especially those involved with ATP generation in muscle.It plays a major role in neurochemical transmission, where itdecreases acetylcholine release and reduces the sensitivity of themotor endplate. Magnesium also improves the contractile responseof the stunned myocardium, and limits infarct size by a mechanismthat has yet to be fully elucidated. 451 The normal plasma range ofmagnesium is 0.8–1.0 mmol l −1 .Hypomagnesaemia is often associated with hypokalaemia, andmay contribute to arrhythmias and cardiac arrest. Hypomagnesaemiaincreases myocardial digoxin uptake and decreasescellular Na+/K + -ATP-ase activity. Patients with hypomagnesaemia,hypokalaemia, or both may become cardiotoxic even with therapeuticdigitalis levels. Magnesium deficiency is not uncommonin hospitalised patients and frequently coexists with otherelectrolyte disturbances, particularly hypokalaemia, hypophosphataemia,hyponatraemia and hypocalcaemia.Although the benefits of giving magnesium in known hypomagnesaemicstates are recognised, the benefit of giving magnesiumroutinely during cardiac arrest is unproven. Studies in adults in andout of hospital 287–291,452 have failed to demonstrate any increasein the rate of ROSC when magnesium is given routinely during CPR.www.elsuapdetodos.comIndications.Magnesium sulphate is indicated in• ventricular or supraventricular tachycardia associated withhypomagnesaemia;• torsades de pointes;• digoxin toxicity.Dose. Give an initial intravenous dose of 2 g (4 ml (8 mmol))of 50% magnesium sulphate) peripherally over 1–2 min; it maybe repeated after 10–15 min. Preparations of magnesium sulphatesolutions differ among European countries.
Clinical aspects of use. Hypokalaemic patients are often hypomagnesaemic.If ventricular tachyarrhythmias arise, intravenousmagnesium is a safe, effective treatment. The role of magnesium inacute myocardial infarction is still in doubt. Magnesium is excretedby the kidneys, but side effects associated with hypermagnesaemiaare rare, even in renal failure. Magnesium inhibits smooth musclecontraction, causing vasodilation and a dose-related hypotension,which is usually transient and responds to intravenous fluids andvasopressors.Other drugsThere is no evidence that routinely giving other drugs (e.g.,atropine, procainamide, bretylium, calcium and hormones) duringhuman cardiac arrest increases survival to hospital discharge.Recommendations for the use of these drugs are based on limitedclinical studies, our understanding of the drug’s pharmacodynamicproperties and the pathophysiology of cardiac arrest.AtropineAtropine antagonises the action of the parasympathetic neurotransmitteracetylcholine at muscarinic receptors. Therefore, itblocks the effect of the vagus nerve on both the sinoatrial (SA) nodeand the atrioventricular (AV) node, increasing sinus automaticityand facilitating AV node conduction.Side effects of atropine are dose-related (blurred vision, drymouth and urinary retention); they are not relevant during acardiac arrest. Acute confusional states may occur after intravenousinjection, particularly in elderly patients. After cardiacarrest, dilated pupils should not be attributed solely to atropine.Asystole during cardiac arrest is usually due to primary myocardialpathology rather than excessive vagal tone and there is noevidence that routine use of atropine is beneficial in the treatmentof asystole or PEA. Several recent studies have failed to demonstrateany benefit from atropine in out-of-hospital or in-hospital cardiacarrests 244,453–458 ; and its routine use for asystole or PEA is no longerrecommended.Atropine is indicated in:• sinus, atrial, or nodal bradycardia when the haemodynamic conditionof the patient is unstable (see Section 4g).CalciumCalcium plays a vital role in the cellular mechanisms underlyingmyocardial contraction. There is no data supporting any beneficialaction for calcium after most cases of cardiac arrest 453,459–463 ;conversely, other studies have suggested a possible adverse effectwhen given routinely during cardiac arrest (all rhythms). 464,465High plasma concentrations achieved after injection may be harmfulto the ischaemic myocardium and may impair cerebral recovery.Give calcium during resuscitation only when indicated specifically,i.e., in pulseless electrical activity caused by• hyperkalaemia;• hypocalcaemia;• overdose of calcium channel-blocking drugs.The initial dose of 10 ml 10% calcium chloride (6.8 mmol Ca 2+ )may be repeated if necessary. Calcium can slow the heart rate andprecipitate arrhythmias. In cardiac arrest, calcium may be givenby rapid intravenous injection. In the presence of a spontaneouscirculation give it slowly. Do not give calcium solutions and sodiumbicarbonate simultaneously by the same route.18 de 0ctubre de 2010 www.elsuapdetodos.comC.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352 1325BuffersCardiac arrest results in combined respiratory and metabolicacidosis because pulmonary gas exchange ceases and cellularmetabolism becomes anaerobic. The best treatment of acidaemiain cardiac arrest is chest compression; some additional benefit isgained by ventilation. During cardiac arrest, arterial gas values maybe misleading and bear little relationship to the tissue acid–basestate 292 ; analysis of central venous blood may provide a betterestimation of tissue pH (see Section 4d). Bicarbonate causes generationof carbon dioxide, which diffuses rapidly into cells. It has thefollowing effects.• It exacerbates intracellular acidosis.• It produces a negative inotropic effect on ischaemic myocardium.• It presents a large, osmotically active, sodium load to an alreadycompromised circulation and brain.• It produces a shift to the left in the oxygen dissociation curve,further inhibiting release of oxygen to the tissues.Mild acidaemia causes vasodilation and can increase cerebralblood flow. Therefore, full correction of the arterial blood pH maytheoretically reduce cerebral blood flow at a particularly criticaltime. As the bicarbonate ion is excreted as carbon dioxide via thelungs, ventilation needs to be increased.Several animal and clinical studies have examined the use ofbuffers during cardiac arrest. Clinical studies using Tribonate ®466or sodium bicarbonate as buffers have failed to demonstrateany advantage. 466–472 Only two studies have found clinicalbenefit, suggesting that EMS systems using sodium bicarbonateearlier and more frequently had significantly higher ROSCand hospital discharge rates and better long-term neurologicaloutcome. 473,474 Animal studies have generally been inconclusive,but some have shown benefit in giving sodium bicarbonate totreat cardiovascular toxicity (hypotension, cardiac arrhythmias)caused by tricyclic antidepressants and other fast sodium channelblockers (Section 8b). 294,475 Giving sodium bicarbonate routinelyduring cardiac arrest and CPR or after return of spontaneouscirculation is not recommended. Consider sodium bicarbonatefor• life-threatening hyperkalaemia;• cardiac arrest associated with hyperkalaemia;• tricyclic overdose.Give 50 mmol (50 ml of an 8.4% solution) of sodium bicarbonateintravenously. Repeat the dose as necessary, but use acid/baseanalysis (either arterial, central venous or marrow aspirate fromIO needle) to guide therapy. Severe tissue damage may be causedby subcutaneous extravasation of concentrated sodium bicarbonate.The solution is incompatible with calcium salts as it causes theprecipitation of calcium carbonate.www.elsuapdetodos.comFibrinolysis during CPRThrombus formation is a common cause of cardiac arrest,most commonly due to acute myocardial ischaemia followingcoronary artery occlusion by thrombus, but occasionally due toa dislodged venous thrombus causing a pulmonary embolism.The use of fibrinolytic drugs to break down coronary arteryand pulmonary artery thrombus has been the subject of severalstudies. Fibrinolytics have also been demonstrated in animalstudies to have beneficial effects on cerebral blood flow duringcardiopulmonary resuscitation, 476,477 and a clinical study hasreported less anoxic encephalopathy after fibrinolytic therapy duringCPR. 478Several studies have examined the use of fibrinolytic therapygiven during non-traumatic cardiac arrest unresponsive to
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